Database Query Results : Allicin (mainly Garlic), , neuroP

AL, Allicin (mainly Garlic): Click to Expand ⟱
Features:
Garlic (Allium sativum L.) (active ingredient- Allicin, an active sulfer compound).

Allicin — a reactive organosulfur thiosulfinate generated in situ when garlic (Allium sativum) tissue is crushed (alliin → allicin via alliinase). Functionally, it behaves as a short-lived electrophilic “reactive sulfur species” that rapidly modifies cellular thiols (e.g., glutathione and cysteine residues on proteins), producing broad redox and stress-signaling effects. Classification: small-molecule phytochemical (organosulfur thiosulfinate). Standard abbreviation(s): AL (common in Nestronics), “allicin”. Source/origin: freshly crushed raw garlic; allicin is not present in intact cloves and is chemically unstable, converting to other organosulfur metabolites after formation.

Primary mechanisms (ranked):

  1. Thiol reactivity and redox disruption: rapid GSH/protein-thiol modification (S-thioallylation), shifting redox buffering and triggering oxidative/electrophilic stress signaling.
  2. Mitochondrial stress and intrinsic apoptosis (context-dependent): ΔΨm disruption, cytochrome-c release, caspase activation, ER stress/UPR engagement (often downstream of redox stress).
  3. Inflammatory transcriptional suppression (context-dependent): inhibition of NF-κB–linked programs and, in some models, STAT3 signaling.
  4. Acetate metabolism constraint (model-dependent): reversible inhibition of acetyl-CoA synthetase activity (ACS/ACSS), potentially impacting acetate→acetyl-CoA flux under metabolic stress.
  5. Growth and invasion signaling attenuation (model-dependent): PI3K/AKT and MAPK network modulation with downstream effects on EMT/MMPs and angiogenic programs (e.g., HIF-1α/VEGF).

Bioavailability / PK relevance: “Allicin exposure” is dominated by formation conditions and rapid chemical/biologic turnover. Many oral preparations deliver alliin/alliinase that may generate allicin after ingestion; measured systemic allicin is typically transient, while downstream allyl-sulfur metabolites (e.g., allyl methyl sulfide–related products) are more detectable. Cooking/processing and GI conditions substantially change allicin bioequivalence versus crushed raw garlic.

In-vitro vs systemic exposure relevance: Many anticancer cell studies use ~50–300 µM allicin; whether such free allicin concentrations are achievable at tumor sites after dietary/supplement intake is uncertain because of rapid thiol quenching and conversion to other sulfur species. Reported biological effects at lower concentrations may still occur locally (GI lumen/mucosa) or via metabolites, but direct extrapolation from high-µM in-vitro dosing is high-risk.

Clinical evidence status: Predominantly preclinical (cell/animal) for anticancer mechanisms; human data are mixed and often evaluate garlic preparations rather than purified allicin, with outcomes confounded by formulation-dependent “allicin bioequivalence” and co-occurring organosulfur compounds (e.g., DADS/DATS/SAMC). Cancer-therapeutic evidence remains inconclusive.

DADS (diallyl disulfide is a sulfur-based anticancer drug generated from garlic)
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."

-Allicin is not present in intact garlic.
-It's formed enzymatically when alliin (a sulfur-containing amino acid) is converted by alliinase when garlic is chopped or crushed.Best consumed raw immediately after crushing (wait 5–10 min before consuming for full conversion)
-Allicin is unstable, degrading within hours into other sulfur compounds (like diallyl disulfide).

-Note half-life reports vary 2.5-90hrs?.
-moderately water-soluble but rapidly degrades/quenched (especially with thiols), so aqueous solutions have limited practical stability : BioAv


Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, 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

Allicin (Garlic) — mechanistic axes relevant to oncology

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Thiol chemistry and redox buffering GSH↓, protein thiols modified; ROS↑ (dose-dependent) Adaptive buffering often stronger; ROS↔/↑ (context-dependent) P Electrophilic/thiol stress that re-wires signaling Central “first-contact” mechanism: allicin rapidly reacts with cysteine/GSH, so many downstream pathway changes are secondary to thiol stress.
2 Mitochondria and intrinsic apoptosis ΔΨm↓, Cyt-c↑, Caspase↑, cl-PARP↑ Typically less apoptosis at matched doses (selectivity varies) R Pro-apoptotic stress execution Frequently downstream of rank #1; selectivity can reflect baseline redox fragility and metabolic state.
3 ER stress and UPR ER stress↑, UPR↑ (model-dependent) UPR↔/↑ (context-dependent) R Proteostasis stress amplification Can couple to Ca²⁺ release, apoptosis, and inflammatory signaling changes.
4 Ca²⁺ signaling Ca²⁺↑ (model-dependent) Ca²⁺↔/↑ (context-dependent) R Stress coupling to mitochondria/ER Often reported as part of the ER–mitochondria stress axis rather than a primary target.
5 NF-κB inflammatory axis NF-κB↓; cytokine programs↓ (context-dependent) Inflammatory tone↓ (context-dependent) G Anti-inflammatory transcriptional suppression May be beneficial in tumor-promoting inflammation contexts; also relevant to platelet/vascular biology.
6 STAT3 signaling STAT3↓ (model-dependent) STAT3↔ (context-dependent) G Reduced survival/proliferation programs Evidence is model-specific; frequently downstream of redox/inflammation modulation.
7 NRF2 antioxidant response NRF2↓ or maladaptive NRF2 response (context-dependent) NRF2↑ (context-dependent) G Differential stress adaptation Reported “cancer vs normal” divergence is plausible but not universal; strongly dose/model dependent.
8 Acetate to acetyl-CoA metabolism ACS/ACSS activity↓ (model-dependent) ACS/ACSS activity↓ (context-dependent) R Limits acetate utilization under stress Primary biochemical evidence exists for acetyl-CoA synthetase inhibition by allicin; translation to tumor-selective ACSS2 targeting is uncertain without exposure confirmation.
9 PI3K/AKT and MAPK network PI3K/AKT↓, ERK/JNK↔/↓ (model-dependent) ↔ (context-dependent) G Reduced growth/survival signaling Commonly reported but typically secondary to upstream stress/redox effects.
10 HIF-1α and angiogenesis HIF-1α↓, VEGF↓ (model-dependent) ↔ (context-dependent) G Anti-angiogenic signaling shift Most supportive data are preclinical; dependent on hypoxia models and dosing.
11 EMT, migration, invasion EMT↓, MMPs↓ (model-dependent) ↔ (context-dependent) G Reduced invasive phenotype Usually downstream of PI3K/MAPK/inflammation rewiring and/or oxidative stress–driven cytostasis.
12 Radiosensitization and chemosensitization Sensitization↑ (context-dependent) Protection↔/↑ (context-dependent) G Stress-based therapeutic interaction Potential bidirectionality: pro-oxidant sensitization in tumors vs antioxidant adaptation in normal tissues depends on schedule and formulation.
13 Clinical Translation Constraint Chemical instability; rapid thiol quenching; formulation-dependent “allicin bioequivalence”; uncertain tumor-site free-allicin exposure; many in-vitro studies use high µM levels; human cancer outcomes largely from heterogeneous garlic preparations rather than purified allicin. Primary constraint is exposure control, not target plausibility.


neuroP, neuroprotective: Click to Expand ⟱
Source:
Type:
Neuroprotective refers to the ability of a substance, intervention, or strategy to preserve the structure and function of nerve cells (neurons) against injury or degeneration.
-While cancer and neurodegenerative processes might seem distinct, there is significant overlap in terms of treatment-related neurotoxicity, shared molecular mechanisms, and the potential for therapies that provide neuroprotection during cancer treatment.
Scientific Papers found: Click to Expand⟱
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.

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/CCNB1↓,
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↓,

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)

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.

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.

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↑,

5355- AL,    Mini-review: The health benefits and applications of allicin
- Review, Var, NA
*BioAv↑, another key property of allicin is its hydrophobicity, which allows it to be absorbed easily through the cell membrane without causing any physical or chemical damage to the phospholipid bilayer, thereby allowing its rapid metabolism to produce pharm
*cardioP↑, Allicin exhibits protective effects in multiple organ systems, including the brain, intestines, lungs, liver, kidneys, prostate, and heart.
*hepatoP↑,
*RenoP↑,
*Half-Life↝, half-life (t1/2)of allicin was 227 min–260 min. Because allicin is eliminated from the body by the respiratory tract, the concentration of allicin in lung tissue is significantly lower than that in the blood
*BioAv↓, We believe that the bioavailability of allicin is relatively low for the following reasons: At first, allicin is characterized by a distinctive garlic odor and chemical instability. It can be easily degraded under room temperature.
*neuroP↑, Neuroprotective activity
*cognitive↑, On the other hand, allicin improves cognitive deficits via Protein kinase R-like endoplasmic reticulum kinase (PERK)/Nuclear factor erythroid-2-related factor 2 (NRF2) signaling pathway and c-Jun N-terminal kinase (JNK) signaling pathways
*ROS↓, They found that allicin suppressed ROS generation and decreased lipid peroxidation in 6-hydroxydopamine (6-OHDA)-induced Pheochromocytoma 12 (PC12) cells
*lipid-P↓,
*DNArepair↑, Allicin not only directly protects DNA, but also indirectly protects DNA through antioxidant activity and regulation of oxidizing enzymes
*ChemoSen↑, Allicin combined with other chemotherapy drugs showed a better anti-cancer effect


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   ROS↓, 1,   ROS↑, 1,  

Cell Death ⓘ

Bcl-2↓, 1,   Casp12↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Fas↑, 1,   p38↑, 1,   Telomerase↓, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,  

Migration ⓘ

p‑FAK↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL8↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   cognitive↑, 1,   neuroP↑, 1,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 5,   Catalase↑, 1,   GSH↑, 3,   GSTs↑, 1,   HO-1↑, 1,   Keap1↓, 1,   lipid-P↓, 3,   MDA↓, 1,   MPO↓, 2,   NRF2↑, 3,   ROS↓, 6,   SOD↑, 3,   TBARS↓, 2,  

Mitochondria & Bioenergetics ⓘ

ATP∅, 1,   Insulin↑, 1,   MMP↓, 1,   mtDam↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   H2S↑, 2,   LDH↓, 3,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 1,   Cyt‑c↓, 1,   iNOS↓, 2,   JNK↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   HSP70/HSPA5↑, 1,  

DNA Damage & Repair ⓘ

DNArepair↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↝, 1,   PKCδ↑, 1,  

Angiogenesis & Vasculature ⓘ

p‑eNOS↑, 1,   NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1β↓, 1,   IL6↓, 2,   Inflam↓, 2,   NF-kB↓, 2,   PGE2↓, 1,   TLR4↓, 2,   TNF-α↓, 2,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

RAAS↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 1,   eff↑, 1,   Half-Life↝, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BP↓, 2,   creat↓, 1,   GutMicro↑, 1,   IL6↓, 2,   LDH↓, 3,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   cardioP↑, 4,   cognitive↑, 3,   hepatoP↑, 2,   memory↑, 2,   neuroP↑, 8,   RenoP↑, 1,  
Total Targets: 68

Scientific Paper Hit Count for: neuroP, neuroprotective
7 Allicin (mainly Garlic)
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:27  Target#:1105  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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