Potentilla chinensis Ser.
Urs-12-en-28-oic acid, 2,3,19-trihydroxy-, (2α,3β)-/Jacarandic acid/tomentic acid/Tormentic acid/(2α,3β)-2,3,19-Trihydroxyurs-12-en-28-oic acid/Euscaphic acid/2,3,19-trihydroxyurs-12-en-28-oic acid
602.7±55.0 °C at 760 mmHg
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For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:13850-16-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Interleukin-1β (IL-1β) accelerates degradation of the cartilage matrix and induces apoptosis of chondrocytes. Tormentic acid (TA) is a triterpene isolated from the stem bark of the Vochysia divergens plant, which has been demonstrated to exert in vitro inhibitory activity against hepatocyte apoptosis. However, the effects of TA on IL‑1β‑induced apoptosis of human chondrocytes remain unclear. Therefore, the present study investigated the in vitro effects of TA on human osteoarthritic chondrocyte apoptosis cultivated in the presence of IL‑1β. Human chondrocytes were pretreated with or without various concentrations of TA and then co‑incubated in the absence or presence of IL‑1β for 24 h. Cell viability was determined using the MTT assay, and cell apoptosis was detected using a Nucleosome ELISA kit. Caspase‑3 activity was detected using a caspase‑3 colorimetric assay kit. The levels of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), Bcl‑2, phosphorylated (p)‑phosphoinositide 3‑kinase (PI3K), PI3K, p‑protein kinase B (Akt) and Akt were measured by western blotting. The results revealed that pretreatment with TA inhibited IL‑1β‑induced cytotoxicity and apoptosis in chondrocytes. In addition, TA pretreatment increased B‑cell lymphoma (Bcl)‑2 expression, and decreased caspase‑3 activity and Bax expressionin human chondrocytes. In addition, pretreatment with TA markedly increased the expression of p‑PI3K and p‑Akt in IL‑1β‑induced chondrocytes. Collectively, these results indicate that TA inhibits IL‑1β‑induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway. Therefore, TA may be considered a potential therapeutic target for the treatment of osteoarthritis.
Tormentic Acid Inhibits IL-1β-induced Chondrocyte Apoptosis by Activating the PI3K/Akt Signaling Pathway
Yang Yang 1 , Yawei Wang 2 , Meng Zhao 3 , Haobo Jia 1 , Bing Li 1 , Dan Xing 1
The pro-inflammatory cytokine interleukin-1beta (IL-1β) plays critical roles in pathogenesis of osteoarthritis (OA). Tormentic acid (TA), a triterpene isolated from Rosa rugosa, has anti-inflammatory activity. However, the anti-inflammatory effect of TA on OA is still unclear. So, in the present study, we examined the effect of TA on IL-1β-induced inflammatory response in primary human OA chondrocytes. Our results demonstrated that TA significantly decreased the IL-1β-stimulated expression of matrix metalloproteinase-3 (MMP-3) and MMP-13. It also inhibited the IL-1β-induced expression of inducible nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the production of NO and prostaglandin E2 (PGE2) in human OA chondrocytes. Furthermore, TA greatly inhibited the IL-1β-induced NF-κB activation. In conclusion, this study is the first to demonstrate the anti-inflammatory activity of TA in human OA chondrocytes. TA significantly inhibits the IL-1β-induced inflammatory response by suppressing the NF-κB signaling pathway. Thus, TA may be a potential agent in the treatment of OA.
chondrocyte; interleukin-1beta (IL-1β); osteoarthritis (OA); tormentic acid (TA).
Yang Yang 1 , Yawei Wang 2 , Yumin Wang 1 , Meng Zhao 3 , Haobo Jia 1 , Bing Li 4 , Dan Xing 5
Tormentic Acid Inhibits IL-1β-Induced Inflammatory Response in Human Osteoarthritic Chondrocytes
Tormentic acid (TA) has been reported to have anticancer, anti-inflammatory and anti-atherogenic properties. However, the effects of TA on neuroinflammation have not been reported. In this study, we investigated whether TA inhibited lipopolysaccharide (LPS)-induced inflammatory response in BV2 microglia cells. BV2 microglia cells were treated with TA for 1h before exposure to LPS. The expression of inducible nitric oxide synthase (iNOS), Cyclooxygenase-2 (COX-2), Nuclear factor κB (NF-κB) and liver X receptor alpha (LXRα) was detected by western blotting. The expression of cytokines Tumor necrosis factor-alpha (TNF-α) and interleukin 1beta (IL-1β) was detected by enzyme-linked immunosorbent assays (ELISA). Results showed that TA inhibited nitric oxide (NO), prostaglandin E2 (PGE2) production by inhibiting iNOS and COX-2 expression. TA also inhibited LPS-induced inflammatory cytokines TNF-α and IL-1β expression. Furthermore, TA could activate LXRα and inhibit LPS-induced NF-κB activation. Knowdown of LXRα reversed the anti-inflammatory effects of TA. In conclusion, our results indicate that TA exerts an anti-inflammatory effect on LPS-stimulated BV2 microglia cells by activating LXRα.
LPS; LXRα; NF-κB; PGE(2); microglia; tormentic acid.
Tormentic Acid Reduces Inflammation in BV-2 Microglia by Activating the Liver X Receptor Alpha
A Ma 1 , Y Wang 2 , Q Zhang 3
2015 Feb 26