3-o-acetyl-beta-boswellic-acid has been researched along with Inflammation* in 2 studies
1 review(s) available for 3-o-acetyl-beta-boswellic-acid and Inflammation
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Plant-derived mPGES-1 inhibitors or suppressors: A new emerging trend in the search for small molecules to combat inflammation.
Inflammation comprises the reaction of the body to injury, in which a series of changes of the terminal vascular bed, blood, and connective tissue tends to eliminate the injurious agent and to repair the damaged tissue. It is a complex process, which involves the release of diverse regulatory mediators. The current anti-inflammatory agents are challenged by multiple side effects and thus, new effective therapies are highly needed. The aim of this review is to summarize the described microsomal prostaglandin E synthase-1 (mPGES-1) inhibitors or transcriptional suppressors from medicinal plants, which could be an ideal approach in the management of inflammatory disorders, but need further clinical trials in order to be ultimately validated. Topics: Animals; Anti-Inflammatory Agents; Biological Products; Drug Discovery; Enzyme Inhibitors; Humans; Inflammation; Plants, Medicinal; Prostaglandin-E Synthases | 2018 |
1 other study(ies) available for 3-o-acetyl-beta-boswellic-acid and Inflammation
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Acetyl-α-boswellic acid and Acetyl-β-boswellic acid protects against caerulein-induced pancreatitis via down-regulating MAPKs in mice.
This study is to investigate the protective effect of Acetyl-α-boswellic acid and Acetyl-β-boswellic mixture(α/β-ABA), which is the active ingredients isolated from Frankincense, on actue pancreatitis and its mechanism. Our experimental results showed that 2 μM α/β-ABA reduced production of NO, TNF-α, IL-6, IL-10 and IL-1β in RAW264.7 cells that were stimulated with lipopolysaccharide (LPS) which indicates its anti-inflammatory role. In pancreatitis model induced by caerulein, intra-gastrical administration of 100 mg/kg α/β-ABA relieved inflammatory cells infiltration significantly and attenuated the serum elevation of amylase TNF-α and IL-6 remarkably in mice. Furthermore, α/β-ABA down-regulated mitogen-activated protein kinase (MAPK) family phosphorylated proteins in pancreas, including phosphorylated p38, ERK1/2 and JNK, to reduce the serum inflammatory factors. Finally, α/β-ABA alleviated the pancreatic edema and inflammatory cell infiltration in pancreatitis mice model. This study suggests that α/β-ABA may be targeted for drug development against pancreatitis via modulating MAPKs pathway. Topics: Animals; Cell Survival; Ceruletide; Cytokines; Disease Models, Animal; Down-Regulation; Edema; Inflammation; Lipopolysaccharides; Mice; Mice, Inbred C57BL; Mitogen-Activated Protein Kinases; Pancreatitis; RAW 264.7 Cells; Triterpenes | 2020 |