Celastrol inhibits tumor necrosis factor-alpha induced proliferation and inflammatory responses in RAW264.7 cells

Chen Guang-fu; Guo Yuan-qing; Wu Yu-tian

doi:10.3969/j.issn.2095-4344.2016.37.012

Abstract：BACKGROUND:Celastrol is one of the active components extracted from the traditional Chinese medicine Celastrus orbiculatus characterized by expel ing the wind and promoting blood circulation and relieving swel ing and pain. <br> OBJECTIVE:To investigate the effects of celastrol on tumor necrosis factor-α(TNF-α) induced proliferation and inflammatory responses in RAW264.7 cel s. <br> METHODS:In vitro inflammatory cel models induced by TNF-α(0, 1, 10, 100μg/L) were treated with celastrol (0.1, 0.5, 1.0, 2.0μmol/L). Interleukin-1β,-6,-8 and prostaglandin E2 in the models were measured by enzyme-linked immunosorbent assay. Cel survival was determined by cel counting kit-8. The inflammatory mediator nitric oxide secretion was detected by nitrate reductase assay. mRNA expressions of inducible nitric oxide synthase, cyclin D1 and cyclin E1 were detected by real-time polymerase chain reaction technique. <br> RESULTS AND CONCLUSION:Significantly increased secretion of interleukin-1β,-6,-8, prostaglandin E2 and nitric oxide, cel proliferation, and mRNA expressions of inducible nitric oxide synthase, cyclin D1 and cyclin E1 were observed after the induction of TNF-α(0.1, 10, 100μg/L) compared with the control group (without the induction of TNF-α) (P<0.05);especial y, 10μg/L of TNF-αexhibited the strongest effects. 0.4μmol/L celastrol significantly suppressed TNF-α-induced release of interleukin-1β,-6,-8, prostaglandin E2 and nitric oxide, cel proliferation, and mRNA expressions of inducible nitric oxide synthase, cyclin D1 and cyclin E1 in RAW264.7 cel s (P<0. 05). Our results demonstrate that celastrol can inhibit TNF-α-induced inflammatory response and proliferation in RAW264.7 cel s.