condition found tbRes List
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↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective,

- Selectivity: Cancer Cells vs Normal Cells


MMP2, metalloproteinase-2: Click to Expand ⟱
Source:
Type:
Matrix metalloproteinase-2 (MMP-2) is an enzyme that plays a significant role in the degradation of extracellular matrix components, which is crucial for various physiological processes, including tissue remodeling, wound healing, and angiogenesis.
Elevated levels of MMP-2 have been associated with poor prognosis in various cancers, including breast, lung, and colorectal cancers.
MMP2 and MMP9: two enzymes are critical to tumor invasion.


Scientific Papers found: Click to Expand⟱
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↓,

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

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↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Results for Effect on Cancer/Diseased Cells:
5HT↓,1,   5LO↓,1,   Akt↓,1,   AMPK↑,1,   angioG↓,2,   AntiCan↑,1,   Apoptosis↑,1,   AR↓,2,   ascitic↓,1,   BioAv↓,1,   BioAv↑,2,   Casp↑,1,   Casp3↑,1,   Casp8↑,1,   CDK2↓,1,   CDK4↓,1,   chemoP↑,1,   ChemoSen↑,2,   COX2↓,2,   CXCR4↓,3,   cycD1↓,2,   cycE↓,1,   Cyt‑c↑,1,   Dose↑,1,   DR4↑,1,   DR5↑,1,   eff↑,4,   ER Stress↑,1,   ERK↓,1,   p‑ERK↓,1,   Glycolysis↓,1,   Half-Life↓,1,   HIF-1↓,1,   IKKα↓,1,   IL1α↓,1,   Inflam↓,1,   JNK↑,1,   LC3B↓,1,   Let-7↑,2,   lipid-P?,1,   MAPK↓,1,   MCP1↓,1,   MIP2↓,1,   miR-200b↑,1,   MMP1↓,2,   MMP2↓,3,   MMP9↓,3,   mTOR↓,1,   NF-kB↓,3,   P21↑,1,   cl‑PARP↑,2,   PDGF↓,1,   p‑PDGFR-BB↓,1,   PI3K↓,2,   PPARα↓,1,   radioP↑,1,   p‑RB1↓,1,   ROS↑,1,   STAT3↓,1,   Tf↓,1,   TOP1↓,1,   TOP2↑,1,   toxicity↓,1,   TumCCA↑,1,   TumCG↓,1,   TumCI↓,1,   TumCMig↓,1,   TumCP↓,1,   VEGF↓,4,   VEGFR2↓,1,   Wnt↓,2,   β-catenin/ZEB1↓,2,  
Total Targets: 72

Results for Effect on Normal Cells:
5LO↓,1,   ALAT↓,1,   AST↓,1,   Ca+2↝,1,   cognitive↑,1,   COX2↓,1,   CRP↓,1,   Dose↝,1,   eff↑,1,   GSH↑,1,   hepatoP↑,1,   HO-1↑,1,   IL6↓,1,   Imm↑,1,   Inflam↓,1,   LDH↑,1,   MAPK↑,1,   MDA↓,1,   neuroP↑,1,   NF-kB↓,1,   NRF2↑,1,   ROS↓,1,   SOD↑,1,   TNF-α↓,2,  
Total Targets: 24

Scientific Paper Hit Count for: MMP2, metalloproteinase-2
3 Boswellia (frankincense)
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:47  Target#:201  State#:%  Dir#:%
wNotes=on sortOrder:rid,rpid

 

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