AL, Allicin (mainly Garlic): Click to Expand ⟱
Features:
Garlic (Allium sativum L.) (active ingredient- Allicin, an active sulfer compound).
Summary:
- Four main organic sulfides in garlic, diallyl disulfide (DADS), diallyl trisulfide (DATS), S-allylmercaptocysteine (SAMC) and allicin.
- Reversible inhibitor of ACSS2.
- may inhibit NF-κB signaling
- induce oxidative stress in cancer cells by generating ROS
- might downregulate STAT3 activation
- Inconclusive evidence for cancer treatment.
- may inhibit platelet aggregation
Allicin is a reactive sulfur species (RSS) [23] with oxidizing properties, and it is able to oxidize thiols in cells, e.g., glutathione and cysteine residues in proteins.
-Allicin is not present in intact garlic; rather, it is formed when garlic is chopped or crushed. -Using crushed or chopped raw garlic or adding garlic at the end of the cooking process (after the heat is reduced) can help preserve its potential allicin content.
"Consumption of alliinase-inhibited cooked garlic was found to give higher than expected allicin bioequivalence, with AMS formation being about 30% (roasted garlic) or 16% (boiled garlic) that of crushed raw garlic."

-Note half-life reports vary 2.5-90hrs?.
-low solubility of apigenin in water : BioAv


Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Casp">Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- PI3K/AKT(Inhibition), JAK/STATs, Wnt/β-catenin, AMPK, MAPK/ERK, and JNK.
- inhibit Growth/Metastases : EMT↓, MMP2↓, MMP9↓, VEGF↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓(not commonly listed as inhibitor), DNMT1↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, FAK↓, ERK↓,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓,
- inhibits Cancer Stem Cells : CSC↓,
- Others: PI3K↓, AKT↓, STAT3, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Allicin has been reported to exhibit a range of effects, including:
Antimicrobial activity: 10-50 μM
Antioxidant activity: 10-100 μM
Anti-inflammatory activity: 20-50 μM
Anticancer activity: 50-100 μM or (50–300uM) (2–5 mg allicin per kilogram of body weight per day)
Cardiovascular health: 20-50 μM

Approximate μM concentrations of allicin that can be achieved:
1 clove of garlic (3g): approximately 10-50 μM of allicin
single clove of garlic may yield about 5–9 mg of allicin,
1 tablespoon of minced garlic (15g): approximately 50-150 μM of allicin
1 cup of chopped garlic (100g): approximately 200-500 μM of allicin
1 tablespoon of chopped garlic chives (15g): approximately 5-20 μM of allicin
1 cup of chopped garlic chives (100g): approximately 20-50 μM of allicin
1 ounce (28g) of garlic microgreens: approximately 50-200 μM of allicin
1 cup of garlic microgreens (100g): approximately 200-500 μM of allicin
1 ounce (28g) of garlic chive microgreens: approximately 20-50 μM of allicin
1 cup of garlic chive microgreens (100g): approximately 50-100 μM of allicin

Allicin is a bioactive compound derived from garlic that has garnered significant interest for its potential anticancer properties through multiple mechanisms, including antioxidant activity, induction of apoptosis, cell cycle arrest, and modulation of key signaling pathways. While regular dietary intake of garlic is associated with cancer prevention benefits, allicin is also being explored as an adjunct to conventional cancer treatments.

Available in supplement tablet/capsule form for example at 2000mg (fresh bulb equilvalent)
IC50 of normal cells it >160mg/mL (large selectivity).
IC50 might be about 12-30ug/ml (approximately 62-185 µM) (which is about 30-90 grams of garlic consumption).
This makes it difficult to consume enough supplements to achieve that level.

Pathways:

ROS Generation and Oxidative Stress (inducing)
• ROS generation is often considered a primary trigger that feeds into downstream pathways (e.g., MAPK activation, mitochondrial membrane permeabilization).
Mitochondrial (Intrinsic) Apoptotic Pathway
• ROS-induced mitochondrial damage can lead to the release of cytochrome c and subsequent activation of caspases (e.g., caspase-9 and caspase-3).
NF-κB Signaling Inhibition (block)
Modulation of MAPK Pathways (e.g., p38 MAPK and JNK)
• ROS generation by allicin can activate stress-responsive kinases such as p38 MAPK and c-Jun N-terminal kinase (JNK).
Inhibition of PI3K/Akt Pathway
ROS levels and PI3K/Akt signaling, with increased oxidative stress often correlating with reduced Akt phosphorylation and activity.

At lower doses, allicin may lead to a modest increase in ROS levels that the cell’s antioxidant defenses (e.g., glutathione, superoxide dismutase) can manage
Scientific Papers found: Click to Expand⟱
2656- AL,    Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics
- in-vitro, Park, PC12
*antiOx↑, Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies.
*Apoptosis↓, allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure
*LDH↓,
ROS↓, Allicin also inhibited ROS generation
*lipid-P↓, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities.
*mtDam↓, These protective effects were associated with suppressed mitochondrial dysfunction,
*MMP↓, as evidenced by decreased MMP collapse and cytochrome c release,
*Cyt‑c↓,
*ATP∅, preserved mitochondrial ATP synthesis,
*Ca+2↝, and the promotion of mitochondrial Ca(2+) buffering capacity
*neuroP↑, allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

1290- AL,    Effect of allicin on the expression of Bcl-2 and Bax protein in LM-8 cells
- in-vitro, OS, LM8
Bcl-2↓,
BAX↑,
Apoptosis↑,
TumCG↓,

1916- AL,    Allicin Bioavailability and Bioequivalence from Garlic Supplements and Garlic Foods
- Review, Nor, NA
*BioAv↝, For enteric tablets, ABB varied from 36–104%
*eff↓, but it was reduced to 22–57% when consumed with a high-protein meal, due to slower gastric emptying.
*BioAv↝, garlic powder capsules gave 26–109%
*BioAv↝, Kwai garlic powder tablets, which have been used in a large number of clinical trials, gave 80% ABB, validating it as representing raw garlic in those trials
*eff↑, Hence, many brands of garlic supplements have been enteric-coated to prevent disintegration in the stomach
*Half-Life∅, Hence, many brands of garlic supplements have been enteric-coated to prevent disintegration in the stomach
*eff↑, all brands of normal tablets gave high allicin bioavailability
*eff↑, Hence, both low-protein and high-protein meals would provide a gastric pH ≥ 4.0 for an ample amount of time for the alliinase in disintegrated normal tablets and capsules to convert most of the alliin to allicin in the stomach.
*Dose∅, Three tablets has been the most common dose used in these trials. The N1 tablets in these trials have been consistently standardized to contain 3.9 mg alliin/tablet and to yield 1.8 mg allicin/tablet
*eff↑, The bioavailability of allicin from garlic powder supplements containing alliin and active alliinase can be as high as that from an equivalent amount of crushed raw garlic containing maximum allicin, when consumed with a meal.

2000- AL,    Exploring the ROS-mediated anti-cancer potential in human triple-negative breast cancer by garlic bulb extract: A source of therapeutically active compounds
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, NA
selectivity↑, The inhibitory effect of ASEE was more pronounced in MDA-MB-231 cells than in MCF-7 cells, however, no substantial cytotoxicity was seen in normal Vero cells.
TumCG?,
*toxicity∅, no substantial cytotoxicity was seen in normal Vero cells
ROS↑, TNBC cells treated with high concentrations of ASEE were found in the late apoptotic stage and exhibited an increase in ROS level and a reduction in MMP
MMP↓,
TumCCA↑, increased the percentage of cells in the G2/M phase
P53↑, ASEE upregulated the p53 and Bax proteins while downregulated the Bcl-2, p-Akt, and p-p38 proteins.
Bcl-2↓,
p‑Akt↓,
p‑p38↓,
*ROS∅, Vero normal cells did not display the unusual morphological alteration and reduction in cell viability. ROS production revealed a 1.21 % ROS level only in control cells that is typically seen in healthy cells.

2462- AL,    Comparison of antiplatelet activity of garlic tablets with cardio-protective dose of aspirin in healthy volunteers: a randomized clinical trial
- Trial, Nor, NA
AntiAg∅, Garlic tablet did not have significant effect on PA at any dose.

2463- AL,    Garlic as an antithrombotic and antiplatelet aggregation agent
- Review, Nor, NA
AntiAg↑, This review suggests that garlic and its preparations have a beneficial effect against thrombosis and have an antiplatelet aggregation property.
other↑, Garlic been shown to inhibit platelet aggregation, both in vivo and in vitro

2557- AL,    Allicin, a naturally occurring antibiotic from garlic, specifically inhibits acetyl-CoA synthetase
- in-vitro, NA, NA
ACSS2↓, Allicin is shown to be a specific inhibitor of the acetyl-CoA synthetases from plants, yeast and mammals.

2558- AL,    Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment
- Review, AD, NA
*AntiCan↑, Allicin has shown anticancer, antimicrobial, antioxidant properties and also serves as an efficient therapeutic agent against cardiovascular diseases
*antiOx↑,
*cardioP↑,
*neuroP↑, present review describes allicin as an antioxidant, and neuroprotective molecule
cognitive↑, that can ameliorate the cognitive abilities in case of neurodegenerative and neuropsychological disorders.
*ROS↓, As an antioxidant, allicin fights the reactive oxygen species (ROS) by downregulation of NOX (NADPH oxidizing) enzymes, it can directly interact to reduce the cellular levels of different types of ROS produced by a variety of peroxidases.
*NOX↓,
*TLR4↓, inhibition of TLR4/MyD88/NF-κB, P38 and JNK pathways.
*NF-kB↓,
*JNK↓,
*AntiAg↑, A low concentration of allicin (0.4 mM) can inhibit the platelet aggregation up to 90%, the impact is significantly higher than of similar concentration of aspirin.
*H2S↑, Allicin decomposes rapidly and undergoes a series of reactions with glutathione resulting in the production of hydrogen sulphide (H2S).
*BP↓, H2S is a gaseous signalling molecule involved in the regulation of blood pressure.
Telomerase↓, Allicin inhibits the activity of telomerase in a dose dependent manner subsequently inhibiting the proliferation in the cancer cells
*Insulin↑, Studies have shown a significant increase in the blood insulin levels after treatment with allicin
BioAv↝, optimum temperature for the activity of alliinase is 33 °C, it operates best at pH 6.5, the enzyme is sensitive to acids [42,43] (Figure 3), enteric-coated formulations of garlic supplements are therefore recommended
*GSH↑, It helps to lower the hyperglycaemic conditions and improves the glutathione and catalase biosynthesis [37,38]
*Catalase↑,

2559- AL,    Effect of the Garlic Pill in comparison with Plavix on Platelet Aggregation and Bleeding Time
- Human, Nor, NA
AntiAg↑, Several studies indicated that garlic can inhibit platelet aggregation
COX2↓, garlic prevents inhibition of platelet aggregation by inhibiting cyclooxygenase activity and thus thromboxane A2 (TXA2) and B2 (TXB2
cardioP↑, Garlic can play an effective role in preventing and treating cardiovascular diseases.

2560- AL,    Effect of garlic on platelet aggregation in humans: a study in healthy subjects and patients with coronary artery disease
- ex-vivo, Nor, NA
*AntiAg↑, Garlic and its components are known to possess antiplatelet activity
BioAv↝, Though garlic components leave the body quickly, a slow build-up of the active ingredients may take place.
Dose↝, Each capsule contained oil equivalent to I g of raw garlic. oil extract of garlic was encapsulated. 2 capsules of garlic three times a day (i.e. 6 capsules/day) for a period of 1 month.

2645- AL,    Allicin improves endoplasmic reticulum stress-related cognitive deficits via PERK/Nrf2 antioxidative signaling pathway
- NA, AD, NA
*neuroP↑, Allicin, a garlic extract, has been demonstrated a protective role in AD model.

2646- AL,    Anti-Cancer Potential of Homemade Fresh Garlic Extract Is Related to Increased Endoplasmic Reticulum Stress
- in-vitro, Pca, DU145 - in-vitro, Melanoma, RPMI-8226
AntiCan↑, simple homemade ethanol-based garlic extract (GE). We show that GE inhibits growth of several different cancer cells in vitro
eff↓, These activities were lost during freeze or vacuum drying, suggesting that the main anti-cancer compounds in GE are volatile.
ChemoSen↑, We found that GE enhanced the activities of chemotherapeutics
ER Stress↑, Our data indicate that the reduced proliferation of the cancer cells treated by GE is at least partly mediated by increased endoplasmic reticulum (ER) stress.
tumCV↓, homemade GE was found to reduce the viability of the two multiple myeloma (MM) cell lines, RPMI-8226 and JJN3, as well as the prostate cancer cell line DU145 in a dose-dependent manner,
DNAdam↑, GE alone slightly increased the percentage of tail DNA (% Tail) (representing cumulative levels of abasic sites, as well as single- and double-strand DNA breaks) measured at day one, compared to untreated cells
GSH∅, We could not detect any changes in cellular GSH levels after treatments with GE
HSP70/HSPA5↓, ; however, in support of increased ER stress after GE treatment, we detected an increased pulldown of HSPA5 (BIP), a member of the Hsp70 family
UPR↑, s leading to the accumulation of unfolded proteins in the ER (also known as GRP78)
β-catenin/ZEB1↓, we also found a reduction in the β-catenin leve
ROS↑, In further support for increased ER stress induced by GE, which will lead to elevated ROS-levels and oxidative stress
HO-2↑, we found a significant increase in proteins activated by and important for regulating cellular ROS levels, e.g., OXR1, Txnl1, Hmox2, and Sirt1
SIRT1↑,
GlucoseCon∅, glucose consumption, as well as lactate secretion, were not changed.
lactateProd∅,
chemoP↑, Garlic is reported to reduce cisplatin-induced nephrotoxicity and oxidative stress

2647- AL,    The Mechanism in Gastric Cancer Chemoprevention by Allicin
- Review, GC, NA
ChemoSen↓, Experiments have shown that allicin can be chemopreventive to gastric cancer
TumCG↓, by inhibiting the growth of cancer cells, arresting cell cycle at G2/M phase, endoplasmic reticulum (ER) stress, and mitochondria-mediated apoptosis, which includes the caspase-dependent/-independent pathways and death receptor pathway.
TumCCA↑,
ER Stress↑,
Apoptosis↑,
Casp↑,
DR5↑, DR5 (death receptor 5) was found to be upregulated following allicin treatment

2648- AL,    Allicin Inhibits Osteosarcoma Growth by Promoting Oxidative Stress and Autophagy via the Inactivation of the lncRNA MALAT1-miR-376a-Wnt/β-Catenin Signaling Pathway
- in-vitro, OS, SaOS2 - in-vivo, OS, NA
ROS↑, Allicin inhibited osteosarcoma growth and promoted oxidative stress and autophagy via MALATI-miR-376a
TumCG↓,
TumAuto↑,
Wnt↓, allicin promotes oxidative stress and autophagy to inhibit osteosarcoma growth by inhibiting the Wnt/β-catenin pathway in vivo and in vitro.
β-catenin/ZEB1↓,
MALAT1↓, Allicin Inhibited OS Growth by Promoting Oxidative Stress and Autophagy via Inactivation of the MALAT1-miR-376a-Wnt/β-Catenin Signal Pathway Axis In Vitro and In Vivo

2655- AL,    Allicin and Digestive System Cancers: From Chemical Structure to Its Therapeutic Opportunities
- Review, GC, NA
TGF-β↓, Allicin can reduce the expression of TGF-2 and its receptor after entering directly into gastric cancer cell
cycD1↓, followed by not only downexpression of cyclinD1, cyclinE, and cyclin-dependent kinase (CDK),
cycE↓,
CDK1↓, cyclin-dependent kinase (CDK)
DNAdam↑, but also causing DNA damage and generating ROS
ROS↑,
BAX↑, Allicin increases the levels of Bax (proapoptotic protein), Bcl-2 (antiapoptotic protein), and JNK
JNK↑,
MMP↓, through reduction in outer mitochondrial membrane potential
p38↑, allicin induces p38 mitogen that could induce the protein kinase (MAPK) and then increase the expression of Fas binding to Fas ligand (Fas L) and finally activate death pathway through activation of cyt C and caspase-8.
MAPK↑,
Fas↑,
Cyt‑c↑,
Casp8↑,
PARP↑, allicin makes caspase-dependent apoptosis through elevating PARP, caspase-3 and caspase-9, which are mediated by enhanced discharging of mitochondria cyt C to the cytosol.
Casp3↑,
Casp9↑,
Ca+2↑, allicin induces apoptosis via increasing the amounts of free Ca2+, ER stress.
ER Stress↑,
P21↑, generating ROS to produce p21 and phospho-p53 (Ser15).
CDK2↓, Then p21 suppressed the CDK-4/6/cyclinD complex, P21-PCNA, P21-CDK2, and subsequently reduced cdk1/cyclinB1 complex for G2/M phase cell cycle arrest
CDK6↑,
TumCCA↑,
CDK4↓, Then p21 suppressed the CDK-4/6/cyclinD complex

1069- AL,    Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling
- vitro+vivo, ESCC, TE1 - vitro+vivo, ESCC, KYSE-510 - in-vitro, Nor, Het-1A
TumCP↓,
LC3‑Ⅱ/LC3‑Ⅰ↑,
p62↓,
p‑AMPK↑,
mTOR↓,
TumAuto↑,
NCOA4↑,
MDA↑,
Iron↑, elevated malondialdehyde and Fe2+ production levels
TumW↓,
TumVol↓,
ATG5↑,
ATG7↑,
TfR1/CD71↓,
FTH1↓, suppressed the expression of ferritin heavy chain 1 (the major intracellular iron-storage protein)
ROS↑,
Iron↑,
Ferroptosis↑,
*toxicity↓, 80 μg/mL allicin for 24 h did not change the viability of Het-1A cells. A slight reduction in cell viability was observed when Het-1A cells were treated with 160 μg/mL allicin for 24 h

2657- AL,    Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases
- Review, CardioV, NA - Review, AD, NA
*Inflam↓, allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others).
*antiOx↑, improving the antioxidant system
*neuroP↑,
*cardioP↑,
*AntiTum↑,
*mtDam↑, Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes.
*HSP70/HSPA5↑, llicin improves mitochondrial function by enhancing the expression of HSP70 and decreasing RAAS activation
*NRF2↑,
*RAAS↓,
*cognitive↑, Allicin enhances the cognitive function of APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice by decreasing the expression levels of Aβ, oxidative stress, and improving mitochondrial function.
*SOD↑, positive effects on cognition in an AD mouse model by administrating a preventive dose of allicin. These effects might be mediated by an increase of SOD and reduction of ROS
*ROS↓,
*NRF2↑, Chronic treatment with allicin increased the expression of NRF2 and targeted downstream of NRF2, such as NADPH, quinone oxidoreductase 1 (NQO1), and γ-glutamyl cysteine synthetase (γ-GCS), in the hippocampus of aged mice
*ER Stress↓, protective effects of 16 weeks of allicin treatment in a rat model of endoplasmic reticulum stress-related cognitive deficits.
*neuroP↑, allicin was able to ameliorate depressive-like behaviors by decreasing neuroinflammation, oxidative stress iron aberrant accumulation,
*memory↑, allicin improved lead acetate-caused learning and memory deficits and decreased the ROS level
*TBARS↓, Oral administration of allicin was able to reduce thiobarbituric reactive substances (TBARS) and myeloperoxidase (MPO) levels, and concurrently increased (SOD) activity, glutathione S-transferase (GST) and glutathione (GSH) levels in a rat model of
*MPO↓,
*SOD↑,
*GSH↑,
*iNOS↓, decreasing the expression of iNOS and increased the phosphorylation of endothelial NOS (eNOS)
*p‑eNOS↑,
*HO-1↑, OSCs upregulate the endogenous antioxidant NRF2 and heme oxygenase-1 (HO-1)

2658- AL,    The Toxic Effect Ways of Allicin on Different Cell Lines
- Review, Var, NA
*antiOx↑, The significant functional act of garlic is its anticancer, antimicrobial, antioxidant, antidiabetic, antifibrinolytic, immune enhancing, antiplatelet collected effect and its possible act in prohibiting cardiovascular illnesses
*AntiAg↑,
*cardioP↑,
Ca+2↑, Sultan et al.[34] stated that allicin is cytotoxic to monocytic leukemia cells (THP-1 cells) and stimulates calcium-linked hemolysis and eryptosis in human red blood cells. Allicin advances calcium grades in cells, reasons to oxidative stress and al
ROS↑, Allicin advances calcium grades in cells, reasons to oxidative stress and also induces CK1a, caspase, p38, mitogen-activated protein kinase
Casp↑,
p38↑,
MAPK↑,
hepatoP↑, Wu et al.[42] clarified that allicin applies hepaprotective action counter to hepatic toxicity of cells
chemoP↑, Throughout with other garlic preparations, aged garlic extract (AGE) has been indicated to have hepatoprotective, immune, improving, anticancer, and chemoprotective actions.

2659- AL,    Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells
- in-vitro, HCC, HT29 - in-vitro, HCC, Caco-2
IL1β↓, Allicin markedly inhibited the spontaneous and TNF-α -induced secretion of IL-1β, IL-8, IP-10 and MIG from the two different cell lines in a dose-dependent manner and suppressed the expression of IL-8 and IL-1β mRNA levels
IL8↓,
Inflam↓, allicin may have the potential to attenuate intestinal inflammation.

2660- AL,    Allicin: A review of its important pharmacological activities
- Review, AD, NA - Review, Var, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,

2661- AL,    Allicin alleviates traumatic brain injury-induced neuroinflammation by enhancing PKC-δ-mediated mitophagy
- in-vivo, Nor, NA
*TNF-α↓, Allicin treatment reduced TNF-α, IL-1β, IL-6, ROS levels, and the expression of NLRP3 and TLR4 proteins in mice with CCI, while IL-4 and IL-10 levels remained unchanged.
*IL1β↓,
*IL6↓,
*ROS↓,
*NLRP3↓,
*TLR4↓,
*PKCδ↑, allicin increased PKC-δ expression and PLS3 phosphorylation in the CL-related mitophagy process in both the CCI and Bv2 cell stretch models.
neuroP↑, allicin reduces mitophagy-related neuroinflammation and further prevents neuronal injury in vitro.

2662- AL,    Allicin inhibits tubular epithelial-myofibroblast transdifferentiation under high glucose conditions in vitro
- in-vitro, Nor, HK-2
*α-SMA↓, Allicin partially reversed the high-glucose-induced increase in α-SMA, vimentin and collagen I expression (P<0.01 at 20 µg/ml), increased the expression of E-cadherin
*Vim↓,
*COL1↓,
*E-cadherin↑,
*TGF-β1↓, and significantly downregulated the high glucose-induced expression of TGF-β1 and p-ERK1/2 in a dose-dependent manner (P<0.05).
*p‑ERK↓,
*EMT↓, suggested that high glucose concentrations induced the EMT of HK-2 cells, and that allicin was able to inhibit the EMT, potentially via regulation of the ERK1/2-TGF-β1 signaling pathway.

2663- AL,    Therapeutic Effect of Allicin on Glioblastoma
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG
BioAv↝, After processing, such as cutting, crushing, chewing, or dehydration, alliinase rapidly breaks down alliin to form allicin. Allicin is immediately decomposed to other organosulfur compounds such as diallyl sulphide (DAS), diallyl disulfide(DADS), and
TumCCA↑, The results show DATS can reduce tumor growth by inhibits cell cycle progression and promotes p53-mediated tumor suppression pathways
P53↑,
HDAC↓, The findings demonstrate that DATS can inhibit U87MG cell growth in vivo by inhibiting HDAC [10].
CSCs↓, Inhibition of cancer stem cells(CSC)
ROS↑, DATS can induce apoptosis by ROS through regulation of Bcl-2 and have anticancer effect on human glioblastoma (U87MG) and neuroblastoma (SH-SY5Y) cells
ChemoSen↑, The most interesting thing is allicin can enhance the sensitivity of TMZ-resistant cells to TMZ by inhibiting MGMT expression.
MGMT↓,

2665- AL,    Anticancerous and Antimicrobial Properties of Garlic
- Review, Var, NA
DNMTs↓, A garlic derivative, S-Allylcysteine (SAC). SAC decreases global DNA methylation and also the levels of 5-methylcytosine, DNMT activity, messenger RNA (mRNA) and protein levels of DNMT1
DNMT1↓,

2666- AL,    Targeting the Interplay of Autophagy and ROS for Cancer Therapy: An Updated Overview on Phytochemicals
- Review, Var, NA
Inflam↓, , anti-inflammatory, anti-cancer, and immune-modulatory activities
AntiCan↑,
ROS↑, allicin treatment led to the accumulation of ROS
MAPK↑, activation of MAPK/JNK
JNK↑,
TumAuto↑, of autophagy in non small cell lung cancer (NSCLC) cells.
other↑, autophagy at a low dose of allicin is cytoprotective
Dose↝, whereas a high dose of allicin leads to autophagic cell death.
MALAT1↓, allicin could considerably induce oxidative stress and autophagy to suppress osteosarcoma growth via inactivating the MALAT1-miR-376a-Wnt/β-catenin axis,
Wnt↓,
β-catenin/ZEB1↓,

2667- AL,    Allicin in Digestive System Cancer: From Biological Effects to Clinical Treatment
- Review, GC, NA
AntiCan↑, Allicin not only protects against tumors but also alleviates the adverse effects of anticancer treatment and enhances the chemotherapeutic response under certain conditions.
ChemoSen↑,
angioG↓, DATS works against tumors by blocking the cell cycle, inhibiting tumor cell proliferation, and inhibiting angiogenesis
chemoP↑,
*GutMicro↑, In addition to against bacteria, allicin has also been shown to modulate the composition of gut microbiota (GM) and increase the diversity of beneficial bacteria in animal models
*antiOx↑, allicin was confirmed to have strong antioxidant properties
other↝, Allicin is a reactive sulfur species (RSS) and a potent thiol-trapping reagent, rapidly reacting with glutathione (GSH) to yield S-allylmercaptoglutathione (GSSA)
GSH↓, Thus, allicin depletes the intracellular GSH pool and reacts with cysteine thiols available in proteins through S-thioallylation
Thiols↓, This reaction is the key to the biological activity of allicin, and the reversible oxidation and reduction of protein-thiols is the core of many processes in cells
*ROS↓, In a hypertrophic heart mouse model, the clearance of intracellular ROS by allicin was measured, and has been shown to reduce the production of ROS and block ROS-dependent ERK1/2, JNK1/2, AKT, NF-κB and Smad signaling, which leads to the inhibition o
*hepatoP↑, Moreover, allicin has been proven to play a hepatoprotective role against acetaminophen (APAP)-induced liver injury by reducing oxidative stress
*Inflam↓, OSCs in garlic has been shown to inhibit the tumor-mediated pro-inflammatory activity by modulating the cytokine pattern in a way that leads to an overall inhibition of NF-κB
*NF-kB↓,

2668- AL,    Allicin enhances the radiosensitivity of colorectal cancer cells via inhibition of NF-κB signaling pathway
- in-vitro, CRC, HCT116
RadioS↑, allicin improves the sensitivity of X-ray radiotherapy in CRC, and its mechanism may be associated with inhibition of NF-κB signaling pathway.
NF-kB↓,

2669- AL,  Rad,    Inhibition of ICAM-1 expression by garlic component, allicin, in gamma-irradiated human vascular endothelial cells via downregulation of the JNK signaling pathway
- in-vitro, Nor, HUVECs
*ICAM-1↓, Allicin significantly inhibited gamma IR-induced surface expression of ICAM-1 and ICAM mRNA in a dose-dependent manner.
*AP-1↓, pretreatment with allicin resulted in the decrease of AP-1 activation and phosphorylation of the c-Jun NH2-terminal kinase (JNK) induced by gamma IR.
*p‑cJun↓,
*radioP↑, may be considered in therapeutic strategies for the management of patients treated with radiation therapy
JNK↓, downregulates gamma IR-induced ICAM-1 expression via inhibition of both AP-1 activation and the JNK pathway

2770- AL,    Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis
- in-vivo, Nor, NA - in-vitro, Nor, NRK52E
*antiOx↑, Allicin may exert anti-apoptotic and antioxidative effects to promote renal function recovery in I/R renal tissues and H/R treated NRK-52E cells.
*RenoP↑,
*MDA↓, Allicin ameliorated the increase in MDA content and the reduction in SOD activity induced by renal IRI in groups D, E and F
*SOD↑,

253- AL,    Allicin inhibits invasion and migration of breast cancer cells through the suppression of VCAM-1: Regulation of association between p65 and ER-α
- in-vitro, BC, MDA-MB-231
TumCMig↓,
ERK↓, Allicin suppressed TNF-α-induced activation of ERK1/2
VCAM-1↓,
NF-kB↓,

232- AL,    A Single Meal Containing Raw, Crushed Garlic Influences Expression of Immunity- and Cancer-Related Genes in Whole Blood of Humans
- Human, Nor, NA
*AhR↑, x2.6 increase
*ARNT↑, x1.8 increase
*Hif1a↑, x1.6 increase (whole blood)
*Jun↑, x1.7 increase, x12@3-6hrs
*NFAT↑,
*NFAM1↑, 3 fold increase
*REL↑, x1.7 increase
*OSM↑, x1.8 increase
*NFAT↑, x1.4 increase NFATC3
*CXCc↑, x1.3 increase CXCL14
*IL2↑, x1.1
*IL6↑, x1.3
*LIF↑, x1.4

233- AL,  5-FU,    Allicin sensitizes hepatocellular cancer cells to anti-tumor activity of 5-fluorouracil through ROS-mediated mitochondrial pathway
- in-vivo, Liver, NA
ROS↑,
MMP↓,
Casp3↑, activated
PARP↑, increase of activated caspase-3 and PARP
Bcl-2↓,

234- AL,    Allicin Induces Anti-human Liver Cancer Cells through the p53 Gene Modulating Apoptosis and Autophagy
- in-vitro, HCC, Hep3B
ROS↑, increased the production of ROS levels at 1, 3, 6 h. I
*toxicity∅, In other study, allicin treatment did not increase the leakage of lactate-dehydrogenase (LDH) of primary rat hepatocytes until 1 mM allicin treated with rat hepatocytes24. For this reason, allicin could be inferred as safe to normal liver cells
MMP↓, Allicin decreased mitochondrial membrane potential
BAX↑,
Bcl-2↓,
AIF↑,
Casp3↑, protein expression levels of caspase-3, -8, -9 increased after allicin treatment
Casp8↑,
Casp9↑,
eff↓, Allicin significantly induced ROS overproduction, whereas NAC pretreatment decreased the ROS induction by allicin exposure in Hep 3B cells
γH2AX↑, significant increase in the expression of γ-H2AX was observed at the initial stages (3, 6 h), but not at the later stages of 12, 24, 48 h
selectivity↑, data suggested that allicin induced apoptosis in p53-deficiency human liver carcinoma cells but caused autophagy in p53-normal function human liver carcinoma cells.
DNA-PK↑, increases production of ROS, triggers DNA damage

235- AL,    Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway
- in-vitro, GBM, U87MG
Apoptosis↑,
Bcl-2↓,
BAX↑,
MAPK↑, mechanisms involved in apoptosis include the mitochondrial pathway, activation of mitogen-activated protein kinases (MAPKs), and caspase cascade and oxidant enzyme system.
p‑ERK↑, In the present study, the level of ERK phosphorylation was increased
ROS↑, ROS are related to allicin-induced apoptosis in the U87MG cells.
eff↓, This study demonstrated that allicin-induced apoptosis was down-regulated by the antioxidant enzyme system

236- AL,    Allicin: Chemistry and Biological Properties
- Analysis, NA, NA
GSH↓, allicin reacts with GSH
Bacteria↓, Antimicrobial
LDL↓, reduction without altering HDL
ROS↑, antioxidant at low doses
NRF2↑,
cognitive↑, by activating the Nrf2-system
memory↑, by activating the Nrf2-system
BP↓, via H2S generation
RNS↓,

239- AL,    Allicin induces apoptosis in gastric cancer cells through activation of both extrinsic and intrinsic pathways
- in-vitro, GC, SGC-7901
Apoptosis↑,
Cyt‑c↑, induced cytochrome c release from the mitochondria
Casp3↑,
Casp8↑,
Casp9↑,
BAX↑,
Fas↑,
tumCV↓, 30ug/ml allicin treatment for 48 h reduced tumor cell viability by 70%
DNAdam↑, such as DNA damage, oxidative stress and heat shock proteins
ROS↑,
Telomerase↓, Allicin was shown to induce apoptosis in gastric cancer cells, partly by decreased telomerase activity (21).

241- AL,    Role of p38 MAPK activation and mitochondrial cytochrome-c release in allicin-induced apoptosis in SK-N-SH cells
- in-vitro, neuroblastoma, SK-N-SH
Casp3↑,
Casp9↑,
p38↑,
MAPK↑,
Cyt‑c↑, mitochondrial release of cytochrome-c
Apoptosis↑, allicin induced a significant apoptosis compared with the control group

245- AL,    Allicin: a promising modulator of apoptosis and survival signaling in cancer
- Review, Var, NA
Fas↑,
Bcl-2↓,
BAX↑,
PI3k/Akt/mTOR↝, Allicin can inhibit excessive autophagy by activating the PI3K/Akt/mTOR and MAPK/ERK/mTOR signaling pathways.
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↓,
*toxicity↓, Allicin-loaded nano-formulations efficiently induce apoptosis in cancer cells while minimizing toxicity to normal cells
Cyt‑c↑, allicin induces the release of cytochrome c from the mitochondria

246- AL,    Allicin induces apoptosis of the MGC-803 human gastric carcinoma cell line through the p38 mitogen-activated protein kinase/caspase-3 signaling pathway
- in-vitro, GC, MGC803
Apoptosis↑,
cl‑Casp3↑,
p38↑, In the present study, the protein expression levels of p38 were gradually enhanced in the MGC-803 cells, in response to treatment with 1 μg/ml allicin for 48 h
tumCV↓,
BAX↑, Bax were increased nearly one-fold, whereas the protein expression levels of Bcl-2 level were decreased >35%.
Bcl-2↑,

247- AL,    Allicin inhibits the invasion of lung adenocarcinoma cells by altering tissue inhibitor of metalloproteinase/matrix metalloproteinase balance via reducing the activity of phosphoinositide 3-kinase/AKT signaling
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
MMP2↓, protein levels of
MMP9↓, protein levels of
TIMP1↑,
TIMP2↑,
p‑Akt↓,
PI3K/Akt↓,

248- AL,    Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway
- in-vitro, GBM, U87MG
Bcl-2↓,
BAX↑,
MAPK↑,
ERK↑,
ROS↑, antioxidant prevented inhibitory effect
p38↑,
JNK↑,

249- AL,    Allicin induces apoptosis of the MGC-803 human gastric carcinoma cell line through the p38 mitogen-activated protein kinase/caspase-3 signaling pathway
- in-vitro, GC, MGC803
Casp3↑,
p38↑,
BAX↑, up one fold
Bcl-2↓, down 35%
p38↑,
MAPK↑,

250- AL,    Allicin Induces p53-Mediated Autophagy in Hep G2 Human Liver Cancer Cells
- in-vitro, Liver, HepG2
P53↓, allicin decreased the level of cytoplasmic p53, the PI3K/mTOR signaling pathway
PI3K↓, decreased the levels of PI3K/mTOR, p-Bcl-2, Bcl-xL, and cytoplasmic p53 in Hep G2 cells.
mTOR↓,
Bcl-2↓,
AMPK↑,
TSC2↑,
Beclin-1↑, llicin increased the levels of Beclin-1, Bad, p-AMPK, TSC2, and Atg7
TumAuto↑, Allicin induced autophagy and increased the formation of autophagosomes and autophagolysosomes in Hep G2 cells.
tumCV↓, Allicin treatment at 35 uM decreased the viability of Hep G2 cells after 12 and 24 h significantly.
ATG7↑,
MMP↓, allicin treatment caused a decrease of MMP of Hep G2 cells and degradation of mitochondria

251- AL,    Inhibition of allicin in Eca109 and EC9706 cells via G2/M phase arrest and mitochondrial apoptosis pathway
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706 - in-vivo, NA, NA
Apoptosis↑,
P53↑,
P21↑,
CHK1↑,
CycB↓,
BAX↑,
Casp3↑,
Casp9↑,
Cyt‑c↑, allicin treatment resulted in Cyt c release from the mitochondria to the cytosol.

231- AL,    Molecular Docking Studies with Garlic Phytochemical Constituents to Inhibit the Human EGFR Protein for Lung Cancer Therapy
- Analysis, Lung, NA
EGFR↓,
ROS↑, pro-oxidants in inflammatory conditions

254- AL,    Allicin and Cancer Hallmarks
- Review, Var, NA
NRF2⇅, 40 nM
BAX↑,
Bcl-2↓,
Fas↑,
MMP↓,
Bax:Bcl2↑,
Cyt‑c↑,
Casp3↑,
Casp12↑,
GSH↓, Allicin can easily penetrate the cell membrane and react with the cellular thiol to transiently deplete the intracellular GSH level, inducing the inhibition of cell cycle progression and growth arrest [98].
TumCCA↑,
ROS↑, An in vitro study indicated that allicin encourages oxidative stress and autophagy in Saos-2 and U2OS (osteosarcoma cells) by modulating the MALATI-miR-376a-Wnt and β-catenin pathway [99].
antiOx↓, As an antioxidant phytochemical, it scavenges reactive oxygen species (ROS) and protects cells from oxidative DNA damage [34].

255- AL,    Allicin induces cell cycle arrest and apoptosis of breast cancer cells in vitro via modulating the p53 pathway
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Apoptosis↑,
P53↑,
Casp3↑,
P53↑,
TPM4↓,

256- AL,  doxoR,    Allicin Overcomes Doxorubicin Resistance of Breast Cancer Cells by Targeting the Nrf2 Pathway
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
NRF2↓,
HO-1↓,
p‑Akt↓,

257- AL,  Cisplatin,    Allicin Overcomes Hypoxia Mediated Cisplatin Resistance in Lung Cancer Cells through ROS Mediated Cell Death Pathway and by Suppressing Hypoxia Inducible Factors
- in-vitro, NSCLC, A549
ROS↑, apoptosis and autophagy pathway in A549 cells by ROS accumulation and facilitating S/G2-M phase arrest in both normoxia as well as hypoxia
HIF-1↓,
E-cadherin↑,
N-cadherin↓,
antiOx↓, ROS trigger cell death when its generation reached toxic threshold level by overcoming the antioxidant capacity of the cell and inducing irreversible oxidative modifications of lipid, protein or DNA [30, 48]
Dose↝, 10μg/ml (LD) and 40μg/ml (HD) allicin for 24hr

544- AL,    Garlic constituents for cancer prevention and therapy: From phytochemistry to novel formulations
Risk↓,
ChemoSideEff↓,
TumCG↓,
NF-kB⇅, alter

545- AL,    Association and mechanism of garlic consumption with gastrointestinal cancer risk: A systematic review and meta‑analysis
Risk↓, reduced cancer risk

546- AL,    Effects of garlic intake on cancer: a systematic review of randomized clinical trials and cohort studies
- Review, NA, NA
Risk↓,
TumVol↓, significant decrease in the number and size of colorectal adenomas

547- AL,    Garlic and Cancer: A Critical Review of the Epidemiologic Literature
- Review, NA, NA
Risk↓,

548- AL,    Aged Garlic and Cancer: A Systematic Review
- Review, NA, NA
Risk↓,

549- AL,    Allicin, a naturally occurring antibiotic from garlic, specifically inhibits acetyl-CoA synthetase
ACSS2↓,

550- AL,    A Review on Anticancer Activities of Garlic (Allium sativum L.)
- Review, NA, NA
ChemoSideEff↓,
other↝, protection from cancer advancement

551- AL,    The Influence of Heating on the Anticancer Properties of Garlic
- Analysis, NA, NA
other↓, heating destroyed garlic's active allyl sulfur compound formation, which may relate to its anticancer properties

1023- AL,    Allicin May Promote Reversal of T-Cell Dysfunction in Periodontitis via the PD-1 Pathway
- in-vitro, NA, NA - Analysis, NA, NA
PD-L1↓, We concluded from the in-silico data that allicin could possibly be an inhibitor of PD-L1.

2576- ART/DHA,  AL,    The Synergistic Anticancer Effect of Artesunate Combined with Allicin in Osteosarcoma Cell Line in Vitro and in Vivo
- in-vitro, OS, MG63 - in-vivo, NA, NA
eff↑, Our results indicated that artesunate and allicin in combination exert synergistic effects on osteosarcoma cell proliferation and apoptosis.
tumCV↓,
Casp3↑, apoptotic rate was significantly increased through caspase-3/9 expression and activity enhancement
Casp9↑,
Apoptosis↑,
TumCG↓, Combination suppresses in vivo tumor growth


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 59

Results for Effect on Cancer/Diseased Cells:
ACSS2↓,2,   AIF↑,1,   p‑Akt↓,3,   AMPK↑,1,   p‑AMPK↑,1,   angioG↓,1,   AntiAg↑,2,   AntiAg∅,1,   AntiCan↑,4,   antiOx↓,2,   Apoptosis↓,1,   Apoptosis↑,9,   ATG5↑,1,   ATG7↑,2,   Bacteria↓,1,   BAX↑,11,   Bax:Bcl2↑,1,   Bcl-2↓,11,   Bcl-2↑,1,   Beclin-1↑,1,   BioAv↝,3,   BP↓,1,   Ca+2↑,2,   cardioP↑,1,   Casp↑,2,   Casp12↑,2,   Casp3↑,12,   cl‑Casp3↑,1,   Casp8↑,5,   Casp9↑,8,   CDK1↓,1,   CDK2↓,1,   CDK4↓,1,   CDK6↑,1,   chemoP↑,4,   ChemoSen↓,1,   ChemoSen↑,3,   ChemoSideEff↓,2,   CHK1↓,1,   CHK1↑,1,   cognitive↑,2,   COX2↓,1,   CSCs↓,1,   CycB↓,2,   cycD1↓,1,   cycE↓,1,   Cyt‑c↑,7,   DNA-PK↑,1,   DNAdam↑,3,   DNMT1↓,1,   DNMTs↓,1,   Dose↝,3,   DR5↑,1,   E-cadherin↑,1,   eff↓,3,   eff↑,1,   EGFR↓,1,   ER Stress↑,3,   ERK↓,1,   ERK↑,1,   p‑ERK↑,1,   p‑FAK↓,1,   Fas↑,5,   Ferroptosis↑,1,   FTH1↓,1,   GlucoseCon∅,1,   GSH↓,4,   GSH∅,1,   HDAC↓,1,   hepatoP↑,1,   HIF-1↓,1,   Hif1a↓,1,   HO-1↓,1,   HO-2↑,1,   HSP70/HSPA5↓,1,   IL1β↓,1,   IL8↓,2,   Inflam↓,2,   Iron↑,2,   JNK↓,1,   JNK↑,3,   lactateProd∅,1,   LC3‑Ⅱ/LC3‑Ⅰ↑,1,   LDL↓,1,   MALAT1↓,2,   MAPK↑,7,   MDA↑,1,   memory↑,1,   MGMT↓,1,   MMP↓,6,   MMP2↓,1,   MMP9↓,1,   mTOR↓,2,   N-cadherin↓,1,   NCOA4↑,1,   neuroP↑,1,   NF-kB↓,2,   NF-kB⇅,1,   NRF2↓,1,   NRF2↑,1,   NRF2⇅,1,   other↓,1,   other↑,2,   other↝,2,   P21↑,3,   p38↑,8,   p‑p38↓,1,   P53↓,1,   P53↑,6,   p62↓,1,   PARP↑,2,   PD-L1↓,1,   PI3K↓,1,   PI3K/Akt↓,1,   PI3k/Akt/mTOR↝,1,   RadioS↑,1,   Risk↓,5,   RNS↓,1,   ROS↓,1,   ROS↑,18,   selectivity↑,2,   SIRT1↑,1,   STAT3↓,1,   Telomerase↓,2,   TfR1/CD71↓,1,   TGF-β↓,1,   Thiols↓,1,   TIMP1↑,1,   TIMP2↑,1,   TPM4↓,1,   TSC2↑,1,   TumAuto↑,4,   TumCCA↑,6,   TumCG?,1,   TumCG↓,5,   TumCMig↓,2,   TumCP↓,1,   tumCV↓,5,   TumVol↓,2,   TumW↓,1,   UPR↑,1,   VCAM-1↓,1,   VEGF↓,1,   VEGFR2↓,1,   Wnt↓,2,   β-catenin/ZEB1↓,3,   γH2AX↑,1,  
Total Targets: 147

Results for Effect on Normal Cells:
AhR↑,1,   Akt↓,1,   ALAT↓,1,   AntiAg↑,3,   AntiCan↑,1,   antiOx↑,8,   AntiTum↑,1,   AP-1↓,1,   Apoptosis↓,1,   ARNT↑,1,   AST↓,1,   ATP∅,1,   BBB↑,1,   BioAv↝,3,   BP↓,2,   Ca+2↝,1,   cardioP↑,4,   Catalase↑,1,   p‑cJun↓,1,   cognitive↑,2,   COL1↓,1,   COX2↓,1,   creat↓,1,   CXCc↑,1,   Cyt‑c↓,1,   Dose∅,1,   E-cadherin↑,1,   eff↓,1,   eff↑,5,   EMT↓,1,   p‑eNOS↑,1,   ER Stress↓,1,   p‑ERK↓,1,   GSH↑,3,   GSTs↑,1,   GutMicro↑,2,   H2S↑,2,   Half-Life↝,1,   Half-Life∅,1,   hepatoP↑,2,   Hif1a↑,1,   HO-1↑,1,   HSP70/HSPA5↑,1,   ICAM-1↓,1,   IL1β↓,1,   IL2↑,1,   IL6↓,2,   IL6↑,1,   Inflam↓,3,   iNOS↓,2,   Insulin↑,1,   JNK↓,1,   Jun↑,1,   Keap1↓,1,   LDH↓,3,   LIF↑,1,   lipid-P↓,2,   MDA↓,2,   memory↑,2,   MMP↓,1,   MPO↓,2,   mtDam↓,1,   mtDam↑,1,   neuroP↑,7,   NF-kB↓,3,   NFAM1↑,1,   NFAT↑,2,   NLRP3↓,1,   NO↓,1,   NOX↓,1,   NRF2↑,3,   OSM↑,1,   other↑,1,   PGE2↓,1,   PI3K↓,1,   PKCδ↑,1,   RAAS↓,1,   radioP↑,1,   REL↑,1,   RenoP↑,1,   ROS↓,6,   ROS∅,1,   SOD↑,4,   TBARS↓,2,   TGF-β1↓,1,   TLR4↓,2,   TNF-α↓,2,   toxicity↓,2,   toxicity∅,2,   Vim↓,1,   α-SMA↓,1,  
Total Targets: 91

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:27  Target#:%  State#:%  Dir#:%
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