Bos, Boswellia (frankincense): Click to Expand ⟱
Features:
Boswellia is an herbal extract from the Boswellia serrata tree that may help reduce inflammation.
May help with rheumatoid arthritis, inflammatory bowel disease, asthma, and cancer.
-Naturally occurring pentacyclic triterpenoids include ursolic acid (UA), oleanolic acid (OA), betulinic acid (BetA), bosewellic acid (BA), Asiatic acid (AA), α-amyrin, celastrol, glycyrrhizin, 18-β-glycyrrhetinic acid, lupeol, escin, madecassic acid, momordin I, platycodon D, pristimerin, saikosaponins, soyasapogenol B, and avicin
Boswellia refers to a group of resinous extracts obtained from Boswellia trees (e.g., Boswellia serrata). Traditionally used in Ayurvedic and traditional Chinese medicine, Boswellia is reputed for its anti-inflammatory, analgesic, and immunomodulatory properties. Its bioactive components—such as boswellic acids.
-Anti-inflammatory Activity (blocking the enzyme 5-lipoxygenase) 5LOX↓,.
-AKBA used to reduce Methionine ***** (help in Methionine reduced diet)
Boswellia extracts are often administered in doses ranging from 300 mg to 1,200 mg per day

AKBA (Acetyl-11-keto-β-boswellic acid) is a bioactive compound derived from Boswellia serrata, a plant used traditionally for its anti-inflammatory properties. (upto 30% AKBA in Boswellia MEGA AKBA)
AKBA also available in Inflasanum @ 90% AKDA (MCSformulas)

-Note half-life reports vary 2.5-90hrs?.
BioAv
Pathways:
- induce or lower ROS production (not consistant increase for cancer cells)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑,
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, VEGF↓, NF-κB↓, CXCR4↓, ERK↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, TOP1↓,
- inhibits angiogenesis↓ : VEGF↓, Notch↓, PDGF↓,
- Others: PI3K↓, AKT↓, STAT">STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective,

- Selectivity: Cancer Cells vs Normal Cells


Scientific Papers found: Click to Expand⟱
1448- Bos,    A triterpenediol from Boswellia serrata induces apoptosis through both the intrinsic and extrinsic apoptotic pathways in human leukemia HL-60 cells
- in-vitro, AML, HL-60
TumCP↓,
Apoptosis↑,
ROS↑, initial events involved massive reactive oxygen species (ROS) and nitric oxide (NO) formation
NO↑,
cl‑Bcl-2↑,
BAX↑, translocation of Bax to mitochondria
MMP↓, loss of mitochondrial membrane potential
Cyt‑c↑, release of cytochrome c to the cytosol
AIF↑, release to the cytosol
Diablo↑, release to the cytosol
survivin↓,
ICAD↓,
Casp↑,
cl‑PARP↑,
DR4↑,
TNFR 1↑,

2779- Bos,    Identification of a natural inhibitor of methionine adenosyltransferase 2A regulating one-carbon metabolism in keratinocytes
- in-vitro, Nor, HaCaT - in-vitro, PSA, NA
*MATs↓, Findings AKBA directly interacts with methionine adenosyltransferase 2A (MAT2A), inhibited its enzyme activity, decreased level of S-adenosylmethionine (SAM) and SAM/SAH ratio, and reprogrammed one‑carbon metabolism in HaCaT cells.
*SAM-e↓,

2778- Bos,    Development, Analytical Characterization, and Bioactivity Evaluation of Boswellia serrata Extract-Layered Double Hydroxide Hybrid Composites
- in-vitro, Nor, NA
*ATP↓, this extract is largely composed of terpene substances that are known to be able to bind to the membrane, thus causing the formation of irreversible pores, and they can lower protein synthesis, reducing ATP consumption
*ROS↓, well-known scavenger ability of the boswellic acids [49,50] was expected to significantly reduce the amount of the cytotoxic oxygen- and nitrogen-derived (ROS)

2777- Bos,    Boswellia serrata Preserves Intestinal Epithelial Barrier from Oxidative and Inflammatory Damage
- in-vitro, IBD, NA
*p‑NF-kB↓, BSE and AKBA pretreatment significantly prevented functional and morphological alterations and also the NF-κB phosphorylation induced by the inflammatory stimuli.
*ROS↓, At the same concentrations BSE and AKBA counteracted the increase of ROS caused by H2O2 exposure.
Inflam↓, BSE, in protecting intestinal epithelial barrier from inflammatory damage and supports its use as safe adjuvant in patients affected by IBD.

2776- Bos,    Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities
- Review, Var, NA
*5LO↓, Arthritis Human primary chondrocytes: 5-LOX↓, TNF-α↓, MMP3↓
*TNF-α↓,
*MMP3↓,
*COX1↓, COX-1↓, Leukotriene synthesis by 5-LOX↓
*COX2↓, Arthritis Human blood in vitro: COX-2↓, PGE2↓, TH1 cytokines↓, TH2 cytokines↑
*PGE2↓,
*Th2↑,
*Catalase↑, Ethanol-induced gastric ulcer: CAT↑, SOD↑, NO↑, PGE-2↑
*SOD↑,
*NO↑,
*PGE2↑,
*IL1β↓, inflammation Human PBMC, murine RAW264.7 macrophages: TNFα↓ IL-1β↓, IL-6↓, Th1 cytokines (IFNγ, IL-12)↓, Th2 cytokines (IL-4, IL-10)↑; iNOS↓, NO↓, phosphorylation of JNK and p38↓
*IL6↓,
*Th1 response↓,
*Th2↑,
*iNOS↓,
*NO↓,
*p‑JNK↓,
*p38↓,
GutMicro↑, colon carcinogenesis: gut microbiota; pAKT↓, GSK3β↓, cyclin D1↓
p‑Akt↓,
GSK‐3β↓,
cycD1↓,
Akt↓, Prostate Ca: AKT and STAT3↓, stemness markers↓, androgen receptor↓, Sp1 promoter binding↓, p21(WAF1/CIP1)↑, cyclin D1↓, cyclin D2↓, DR5↑,CHOP↑, caspases-3/-8↑, PARP cleavage, NFκB↓, IKK↓, Bcl-2↓, Bcl-xL↓, caspase 3↑, DNA
STAT3↓,
CSCs↓,
AR↓,
P21↑,
DR5↑,
CHOP↑,
Casp3↑,
Casp8↑,
cl‑PARP↑,
DNAdam↑,
p‑RB1↓, Glioblastoma: pRB↓, FOXM1↓, PLK1↓, Aurora B/TOP2A pathway↓,CDC25C↓, pCDK1↓, cyclinB1↓, Aurora B↓, TOP2A↓, pERK-1/-2↓
Foxm1↓,
TOP2↓,
CDC25↓,
p‑CDK1↓,
p‑ERK↓,
MMP9↓, Pancreas Ca: Ki-67↓, CD31↓, COX-2↓, MMP-9↓, CXCR4↓, VEGF↓
VEGF↓,
angioG↓, Apoptosis↑, G2/M arrest, angiogenesis↓
ROS↑, ROS↑,
Cyt‑c↑, Leukemia : cytochrome c↑, AIF↑, SMAC/DIABLO↑, survivin↓, ICAD↓
AIF↑,
Diablo↑,
survivin↓,
ICAD↓,
ChemoSen↑, Breast Ca: enhancement in combination with doxorubicin
SOX9↓, SOX9↓
ER Stress↑, Cervix Ca : ER-stress protein GRP78↑, CHOP↑, calpain↑
GRP78/BiP↑,
cal2↓,
AMPK↓, Breast Ca: AMPK/mTOR signaling↓
mTOR↓,
ROS↓, Boswellia extracts and its phytochemicals reduced oxidative stress (in terms of inhibition of ROS and RNS generation)

2775- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
ROS↑, modulation of reactive oxygen species (ROS) formation and the resulting endoplasmic reticulum stress is central to BA’s molecular and cellular anticancer activities
ER Stress↑,
TumCG↓, Cell cycle arrest, growth inhibition, apoptosis induction, and control of inflammation are all the effects of BA’s altered gene expression
Apoptosis↑,
Inflam↓,
ChemoSen↑, BA has additional synergistic effects, increasing both the sensitivity and cytotoxicity of doxorubicin and cisplatin
Casp↑, BA decreases viability and induces apoptosis by activat- ing the caspase-dependent pathway in human pancreatic cancer (PC) cell lines
ERK↓, BA might inhibit the activation of Ak strain transforming (Akt) and extracellular signal–regulated kinase (ERK)1/2,
cl‑PARP↑, initiation of cleavage of PARP were prompted by the treatment with AKBA
AR↓, AKBA affects the androgen receptor by reducing its expression,
cycD1↓, decrease in cyclin D1, which inhibits cellular proliferation
VEGFR2↓, In prostate cancer, the downregulation of vascular endothelial growth factor receptor 2–mediated angiogenesis caused by BA
CXCR4↓, Figure 6
radioP↑,
NF-kB↓,
VEGF↓,
P21↑,
Wnt↓,
β-catenin/ZEB1↓,
Cyt‑c↑,
MMP2↓,
MMP1↓,
MMP9↓,
PI3K↓,
MAPK↓,
JNK↑,
*5LO↓, Table 1 (non cancer)
*NRF2↑,
*HO-1↑,
*MDA↓,
*SOD↑,
*hepatoP↑, Preclinical studies demonstrated hepatoprotective impact for BA against different models of hepatotoxicity via tackling oxidative stress, and inflammatory and apoptotic indices
*ALAT↓,
*AST↓,
*LDH↑,
*CRP↓,
*COX2↓,
*GSH↑,
*ROS↓,
*Imm↑, oral administration of biopolymeric fraction (BOS 200) from B. serrata in mice led to immunostimulatory effects
*Dose↝, BA at low concentration tend to stimulate an immune response, as those utilized in the study of Beghelli et al. (2017) however, utilizing higher concentration suppressed the immune response
*eff↑, Useful actions on skin and psoriasis
*neuroP↑, AKBA has substantially diminished the levels of inflammatory markers such as 5-LOX, TNF-, IL-6, and meliorated cognition in lipopolysaccharide-induced neuroinflammation rodent models
*cognitive↑,
*IL6↓,
*TNF-α↓,

2774- Bos,    Boswellia ovalifoliolata abrogates ROS mediated NF-κB activation, causes apoptosis and chemosensitization in Triple Negative Breast Cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-453
ChemoSen↑, BL EthOH has synergistic chemosensitizing effects on TNBC cells and increased the cytotoxicity of doxorubicin and cisplatin
Casp3↑, BL EthOH caused 5 folds and 6 folds increase of caspase 3 levels in both MDA-MB-231 and MDA-MB-453 cells respectively when compared with the untreated control cells
ROS↓, treatment with plant extract significantly inhibited the H 2 O2 induced ROS generation in both MDA-MB-231 and MDA-MB-453 cells.
NF-kB↓, The expression of phospho-NF-kB (ser536) decreased dose dependently in MDA-MB-231and MDA-MB-453cells after treatment with BL EthOH.

2773- Bos,    Targeted inhibition of tumor proliferation, survival, and metastasis by pentacyclic triterpenoids: Potential role in prevention and therapy of cancer
- Review, Var, NA
Inflam↓, BA has been shown to be effective against chronic inflammation-driven diseases such as adjuvant or bovine serum albumin-induced arthritis, osteoarthritis, Crohn’s disease, ulcerative colitis, and ileitis, and galactosamine/endotoxin-induced hepa
TumCCA↑, BA induced apoptosis was mediated by cell cycle arrest in the G1 phase and by activating caspases 3, 8 and 9 in HT-29 cells
Casp3↑,
Casp8↑,
Casp9↑,
STAT3↑, BA inhibited the growth of multiple myeloma cells by suppression of STAT3 pathway and by activation of protein tyrosine phosphatase SHP1
SHP1↓,
NF-kB↓, BA down regulated the expression of NF-kB, cyclin D1, COX2, Ki-67, CD-31 and IAPs in the tumor tissue.
cycD1↓,
COX2↓,
Ki-67↓,
CD31↓,
IAP1↓,
MMPs↓, AKBA induced cell cycle arrest was mediated by down-regulating the expression of cyclinD1, suppresses MMP activity, and also induced apoptosis by suppressing Bcl-2, and Bcl-xL expression
Bcl-2↓,
Bcl-xL↓,

2772- Bos,    Mechanistic role of boswellic acids in Alzheimer’s disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, (AKBA) that possess potent anti-inflammatory and neuroprotective properties in AD
*Inflam↓,
*AChE↓, inhibiting the acetylcholinesterase (AChE) activity in the cholinergic pathway and improve choline levels
*Choline↑,
*NRF2↑, BAs modulate key molecular targets and signalling pathways like 5-lipoxygenase/cyclooxygenase, Nrf2, NF-kB, cholinergic, amyloid-beta (Aβ), and neurofibrillary tangles formation (NFTs) that are involved in AD
*NF-kB↑,
*BBB↑, AKBA has efficiently abled to cross the blood brain barrier (BBB)
*BioAv↑, bioavailability of AKBA was significantly higher in case of sublingual route when compared to intranasal administration, as demonstrated by area under curves (AUCs) analysis
*Half-Life↓, half-life of the drug was about six hours and peak plasma levels of the drug reach 30 hrs after oral administration of 333 mg of BSE.
*Dose↝, drug needs to be administered at a dosing interval of 6 hrs
*PGE2↓, BAs possessed anti-inflammatory activity by inhibiting microsomal prostaglandin E2 synthase-1 (mPGES1)
*ROS↓, prevented oxidative stress-induced neuronal damage and cognitive impairment because of the antioxidant, anti-inflammatory and anti-glutamatergic effects
*cognitive↑,
*antiOx↑,
5LO↓, AKBA significantly reduced pro-inflammatory mediators such as 5-LOX, TNF-α, IL-6 levels and improve cognition
*TNF-α↓,
*IL6↓,
*HO-1↑, AKBA shows neuroprotective effects against ischaemic injury via nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) cascade activation

2768- Bos,    Boswellic acids as promising agents for the management of brain diseases
- Review, Var, NA - Review, AD, NA - Review, Park, NA
*neuroP↑, BAs-induced neuroprotection is proposed to be associated with the ability to reduce neurotoxic aggregates, decrease oxidative stress, and improve cognitive dysfunction.
*ROS↓,
*cognitive↓,
TumCP↓, BAs have been suggested as potential agents for the treatment of brain tumors due to their potential to attenuate cell proliferation, migration, metastasis, angiogenesis, and promote apoptosis during both in vitro and in vivo studies
TumCMig↓,
TumMeta↓,
angioG↓,
Apoptosis↑,
*Inflam↓, The anti-inflammatory activities of BAs have been investigated in many preclinical and clinical trials
IL1↓, BAs inhibit the production of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-2, IL-4, IL-6, and tumor necrosis factor-α (TNF-α) in several experimental studies.
IL2↓,
IL4↓,
IL6↓,
TNF-α↓,
P53↑, AKBA has been reported to induce apoptosis in pancreatic and gastric cancers, through tumor suppressor protein 53 (p53)-independent pathway, while reducing expression of protein kinase (PK) B and NF-kb
Akt↓,
NF-kB↓,
DNAdam↑, DNA fragmentation, and activation of caspase cascade
Casp↑,
COX2↓, regulated genes such as cyclooxygenase-2 (COX-2), matrix metallopeptidase-9 (MMP-9), C-X-C motif chemokine receptor 4 (CXCR4), and vascular endothelial growth factor (VEGF)
MMP9↓,
CXCR4↓,
VEGF↓,
*SOD↑, BAs against oxidative injury has been shown in several cell lines and animal models [12], [13], [21]. BAs exert protective effects through the normalization of antioxidant enzyme levels, such as superoxide dismutase (SOD), catalase, and glutathione p
*Catalase↑,
*GPx↑,
*NRF2↑, Moreover, it can activate nuclear factor erythroid 2-related factor-2 (Nrf2)/antioxidant response element-regulated pathways

2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoP↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2 pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer

2024- Bos,    Antiproliferative and cell cycle arrest potentials of 3-O-acetyl-11-keto-β-boswellic acid against MCF-7 cells in vitro
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
MMP↓, mitochondrial membrane potential (ΔΨm) was reduced by increasing AKBA concentration with a significant release of cytochrome c.
Cyt‑c↑,
ROS↑, A significant increase in reactive oxygen species formation was observed. Compared with the untreated control, 1.32-, 1.61- and 2.44-fold ROS generation increases were achieved following 50, 100 and 200 µg mL−1 AKBA
Casp8↑, activated the production of caspase 8 and caspase 9 in a dose-dependent pattern
Casp9↑,
AntiTum↑, antitumoral activity against MCF-7 cells in a dose-dependent pattern with a reduction rate of 21.65 ± 6.63, 32.37 ± 6.97, 54.29 ± 5.35 and 61.42 ± 4.14% for the concentrations 50, 100, 200 and 400 µg mL−1, respectively
selectivity↑, cell inhibition rate with calculated IC50 of 101.1 and 275.2 for MCF-7 and MCF-10A, respectively
TumCCA↑, finally arrested the MCF-7 cell cycle at the G1 phase.

1451- Bos,    Phytochemical Analysis and Anti-cancer Investigation of Boswellia serrata Bioactive Constituents In Vitro
- in-vitro, CRC, HepG2 - in-vitro, CRC, HCT116
eff↑, HepG2 cell line, extracts 1 and 2 elicited the most pronounced cytotoxic activity with IC50 values equal 1.58 and 5.82 μg/mL at 48 h, respectively which were comparable to doxorubicin with an IC50 equal 4.68 μg/mL at 48 h.

1450- Bos,  Cisplatin,    3-Acetyl-11-keto-β-boswellic acid (AKBA) induced antiproliferative effect by suppressing Notch signaling pathway and synergistic interaction with cisplatin against prostate cancer cells
- in-vitro, Pca, DU145
ROS↑, increased reactive oxygen species (ROS) generation
MMP↓,
Casp↑,
Apoptosis↑,
Bax:Bcl2↑,
TumCCA?, induce G0/G1 arrest
cycD1↓,
CDK4↓,
P21↑,
p27↑,
NOTCH↓, AKBA demonstrated significant downregulation of Notch signaling mediators
ChemoSen↑, AKBA has the potential to synergistically enhance the cytotoxic efficacy of cisplatin

1449- Bos,  Chemo,    Anti-proliferative, Pro-apoptotic, and Chemosensitizing Potential of 3-Acetyl-11-keto-β-boswellic Acid (AKBA) Against Prostate Cancer Cells
- in-vitro, Pca, PC3
TumCP↓,
ChemoSen↑, AKBA was also found to chemosensitize PC3 cells in synergistic combination with doxorubicin.
MMP↝,
ROS↝,
Apoptosis↑,

1169- Bos,    Boswellic Acid Inhibits Growth and Metastasis of Human Colorectal Cancer in Orthotopic Mouse Model By Downregulating Inflammatory, Proliferative, Invasive, and Angiogenic Biomarkers
- in-vivo, CRC, NA
TumCG↓,
TumVol↓,
Weight∅, without significant decreases in body weight
ascitic↓,
TumMeta↓,
Ki-67↓,
CD31↓,
NF-kB↓,
COX2↓,
Bcl-2↓,
Bcl-xL↓,
IAP1↓,
survivin↓,
cycD1↓,
ICAM-1↓,
MMP9↓,
CXCR4↓,
VEGF↓,

1447- Bos,    Boswellia carterii n-hexane extract suppresses breast cancer growth via induction of ferroptosis by downregulated GPX4 and upregulated transferrin
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vivo, BC, 4T1 - in-vitro, Nor, MCF10
tumCV↓,
AntiCan↑, BCHE exhibited potent anti-BC activity in vivo
*toxicity↓, no significant toxic effects
Ferroptosis↑,
i-Iron↑, intracellular accumulation of Fe2+
GPx4↓,
ROS↑, upregulation of reactive oxygen species
lipid-P↑, induced lipid peroxidation in BC cells
Tf↑, Transferrin upregulation in tumor-bearing mice
TumCG↓,

1427- Bos,    Acetyl-keto-β-boswellic acid inhibits cellular proliferation through a p21-dependent pathway in colon cancer cells
- in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116 - in-vitro, CRC, LS174T
TumCG↓,
TumCCA↑, G1 phase
cycD1↓,
cycE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
P21↑,

1426- Bos,  CUR,  Chemo,    Novel evidence for curcumin and boswellic acid induced chemoprevention through regulation of miR-34a and miR-27a in colorectal cancer
- in-vivo, CRC, NA - in-vitro, CRC, HCT116 - in-vitro, CRC, RKO - in-vitro, CRC, SW480 - in-vitro, RCC, SW-620 - in-vitro, RCC, HT-29 - in-vitro, CRC, Caco-2
miR-34a↑, curcumin and AKBA induced upregulation of tumor-suppressive miR-34a and downregulation of miR-27a in CRC cells
miR-27a-3p↓,
TumCG↓,
BAX↑,
Bcl-2↓,
PARP1↓,
TumCCA↑,
Apoptosis↑,
cMyc↓,
CDK4↓,
CDK6↓,
cycD1↓,
ChemoSen↑, combined treatment further increased the inhibitory effects
miR-34a↑, miR-34a expression was upregulated by curcumin and further elevated by concurrent treatment with curcumin and AKBA in HCT116 cell
miR-27a-3p↓,

1425- Bos,    Protective Effect of Boswellic Acids against Doxorubicin-Induced Hepatotoxicity: Impact on Nrf2/HO-1 Defense Pathway
- in-vivo, Nor, NA
*ChemoSen↑, BAs significantly improved the altered liver enzyme activities and oxidative stress markers.
*NRF2↑, BAs increased the Nrf2 and HO-1 expression, which provided protection against DOX-induced oxidative insult
*HO-1↑,
*ROS↓, appear to scavenge ROS and inhibit lipid peroxidation and DNA damage of DOX-induced hepatotoxicity
*lipid-P↓,
*DNAdam↓,

1424- Bos,    Boswellia sacra essential oil induces tumor cell-specific apoptosis and suppresses tumor aggressiveness in cultured human breast cancer cells
- in-vitro, BC, T47D - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
tumCV↓,
Apoptosis↑,
cl‑Casp8↑, MDA-MB-231
cl‑Casp9↑, MDA-MB-231
cl‑PARP↑, MDA-MB-231

1423- Bos,    Acetyl-11-keto-β-Boswellic Acid Suppresses Invasion of Pancreatic Cancer Cells Through The Downregulation of CXCR4 Chemokine Receptor Expression
- in-vitro, Melanoma, U266 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, SkBr3 - in-vitro, PC, PANC1
CXCR4↓, AKBA is a novel inhibitor of CXCR4 expression
TumCI↓,
HER2/EBBR2↓, AKBA downregulated the expression of HER2 in all pancreatic cancer cells, but not in all breast cancer cell lines.
NF-kB↓,

1422- Bos,    Boswellic acid exerts antitumor effects in colorectal cancer cells by modulating expression of the let-7 and miR-200 microRNA family
- in-vitro, CRC, NA - in-vivo, NA, NA
5LO↓, boswellic acids, is known to be a non-redox and non-competitive inhibitor of 5-lipoxygenase
TumCG↓,
Let-7↑,
miR-200b↑, AKBA significantly up-regulated expression of the let-7 and miR-200 families in various CRC cell lines
NF-kB↓,
cMyc↓,
cycD1↓,
MMP9↓,
CXCR4↓,
VEGF↓,
Bcl-xL↓,
survivin↓,
IAP1↓,
XIAP↓,
TumCG↓,
CDK6↓,
Vim↓,
E-cadherin↑,

1421- Bos,    Coupling of boswellic acid-induced Ca2+ mobilisation and MAPK activation to lipid metabolism and peroxide formation in human leucocytes
- in-vitro, AML, HL-60 - in-vitro, Nor, NA
ROS↑, AKBA and KBA strongly upregulated the formation of ROS, whereas β-BA and A-β-BA had only moderate effects
NADPH↝, AKBA-induced ROS formation involves NADPH oxidase, PI 3-K, and p42/44MAPK, and requires Ca2+
5LO↓, With respect to inhibition of 5-LO, 3-acetyl-11-keto-BA (AKBA) was the most potent BA, whereas BAs lacking an 11-keto-group were weak 5-LO inhibitor s
Ca+2↑, 11-keto-BAs potently stimulate the elevation of intracellular Ca2+ levels and activate p38 MAPK as well as p42MAPK
p38↑,
p42↑,

1420- Bos,    Acetyl-11-keto-β-boswellic acid inhibits proliferation and induces apoptosis of gastric cancer cells through the phosphatase and tensin homolog /Akt/ cyclooxygenase-2 signaling pathway
- vitro+vivo, GC, BGC-823
TumCP↓,
TumCG↓, vivo
PTEN↑,
BAX↑,
Bcl-2↓,
p‑Akt↓,
COX2↓,

1419- Bos,    Enhanced Bioavailability of Boswellic Acid by Piper longum: A Computational and Pharmacokinetic Study
- in-vivo, Nor, NA
*BioAv↑, Piper longum extract at 2.5 and 10 mg/kg, increased the bioavailability of Boswellic acid

1417- Bos,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
5LO↓,
COX2↓,
PGE2↓,

1416- Bos,    Anti-cancer properties of boswellic acids: mechanism of action as anti-cancerous agent
- Review, NA, NA
5LO↓,
TumCCA↑, G0/G1 phase
LC3B↓, reduced the expression of LC3A/B-I and LC3A/B-II,
PI3K↓,
Akt↓,
Glycolysis↓,
AMPK↑,
mTOR↓,
Let-7↑,
COX2↓, methanolic extract decreased the expression of cyclooxygenase-2 gene
VEGF↓,
CXCR4↓,
MMP2↓,
MMP9↓,
HIF-1↓,
angioG↓,
TumCP↓,
TumCMig↓,
NF-kB↓,

1248- Bos,    The anti-proliferative effects of a frankincense extract in a window of opportunity phase ia clinical trial for patients with breast cancer
- Trial, BC, NA
TumCP↓, In the B. serrata-treated group there was a reduction in proliferation between core biopsy and excision

1185- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, NA, NA
BAX↑,
NF-kB↓,
cl‑PARP↑,
Casp3↑,
Casp8↑,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 30

Results for Effect on Cancer/Diseased Cells:
5HT↓,1,   5LO↓,5,   AIF↑,2,   Akt↓,3,   p‑Akt↓,2,   AMPK↓,1,   AMPK↑,1,   angioG↓,4,   AntiCan↑,2,   AntiTum↑,1,   Apoptosis↑,7,   AR↓,3,   ascitic↓,2,   BAX↑,4,   Bax:Bcl2↑,1,   Bcl-2↓,4,   cl‑Bcl-2↑,1,   Bcl-xL↓,3,   BioAv↓,1,   BioAv↑,2,   Ca+2↑,1,   cal2↓,1,   Casp↑,4,   Casp3↑,5,   Casp8↑,5,   cl‑Casp8↑,1,   Casp9↑,2,   cl‑Casp9↑,1,   CD31↓,2,   CDC25↓,1,   p‑CDK1↓,1,   CDK2↓,2,   CDK4↓,4,   CDK6↓,2,   chemoP↑,1,   ChemoSen↑,7,   CHOP↑,1,   cMyc↓,2,   COX2↓,7,   CSCs↓,1,   CXCR4↓,7,   cycD1↓,9,   cycE↓,2,   Cyt‑c↑,4,   Diablo↑,2,   DNAdam↑,2,   Dose↑,1,   DR4↑,2,   DR5↑,2,   E-cadherin↑,1,   eff↑,5,   ER Stress↑,2,   ERK↓,1,   p‑ERK↓,2,   Ferroptosis↑,1,   Foxm1↓,1,   Glycolysis↓,1,   GPx4↓,1,   GRP78/BiP↑,1,   GSK‐3β↓,1,   GutMicro↑,1,   Half-Life↓,1,   HER2/EBBR2↓,1,   HIF-1↓,1,   IAP1↓,3,   ICAD↓,2,   ICAM-1↓,1,   IKKα↓,1,   IL1↓,1,   IL1α↓,1,   IL2↓,1,   IL4↓,1,   IL6↓,1,   Inflam↓,3,   i-Iron↑,1,   JNK↑,1,   Ki-67↓,2,   LC3B↓,1,   Let-7↑,3,   lipid-P?,1,   lipid-P↑,1,   MAPK↓,1,   MCP1↓,1,   MIP2↓,1,   miR-200b↑,2,   miR-27a-3p↓,2,   miR-34a↑,2,   MMP↓,3,   MMP↝,1,   MMP1↓,2,   MMP2↓,3,   MMP9↓,7,   MMPs↓,1,   mTOR↓,2,   NADPH↝,1,   NF-kB↓,10,   NO↑,1,   NOTCH↓,1,   P21↑,4,   p27↑,1,   p38↑,1,   p42↑,1,   P53↑,1,   cl‑PARP↑,6,   PARP1↓,1,   PDGF↓,1,   p‑PDGFR-BB↓,1,   PGE2↓,1,   PI3K↓,2,   PPARα↓,1,   PTEN↑,1,   radioP↑,1,   p‑RB1↓,3,   ROS↓,2,   ROS↑,7,   ROS↝,1,   selectivity↑,1,   SHP1↓,1,   SOX9↓,1,   STAT3↓,2,   STAT3↑,1,   survivin↓,4,   Tf↓,1,   Tf↑,1,   TNF-α↓,1,   TNFR 1↑,1,   TOP1↓,1,   TOP2↓,1,   TOP2↑,1,   toxicity↓,1,   TumCCA?,1,   TumCCA↑,5,   TumCG↓,8,   TumCI↓,2,   TumCMig↓,2,   TumCP↓,6,   tumCV↓,2,   TumMeta↓,2,   TumVol↓,1,   VEGF↓,8,   VEGFR2↓,1,   Vim↓,1,   Weight∅,1,   Wnt↓,2,   XIAP↓,1,   β-catenin/ZEB1↓,2,  
Total Targets: 146

Results for Effect on Normal Cells:
5LO↓,2,   AChE↓,1,   ALAT↓,1,   antiOx↑,1,   AST↓,1,   ATP↓,1,   BBB↑,1,   BioAv↑,2,   Ca+2↝,1,   Catalase↑,2,   ChemoSen↑,1,   Choline↑,1,   cognitive↓,1,   cognitive↑,2,   COX1↓,1,   COX2↓,2,   CRP↓,1,   DNAdam↓,1,   Dose↝,2,   eff↑,1,   GPx↑,1,   GSH↑,1,   Half-Life↓,1,   hepatoP↑,1,   HO-1↑,3,   IL1β↓,1,   IL6↓,3,   Imm↑,1,   Inflam↓,3,   iNOS↓,1,   p‑JNK↓,1,   LDH↑,1,   lipid-P↓,1,   MAPK↑,1,   MATs↓,1,   MDA↓,1,   MMP3↓,1,   neuroP↑,3,   NF-kB↓,1,   NF-kB↑,1,   p‑NF-kB↓,1,   NO↓,1,   NO↑,1,   NRF2↑,4,   p38↓,1,   PGE2↓,2,   PGE2↑,1,   ROS↓,6,   SAM-e↓,1,   SOD↑,3,   Th1 response↓,1,   Th2↑,2,   TNF-α↓,4,   toxicity↓,1,  
Total Targets: 54

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:47  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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