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OBJECTIVE To investigate the effects of ex-tract of Ramulus Cinnamom(RC)against LPS-induced inflammation in microglia.METHODS Activated microglia releases various pro-inflammatory cytokines to induce neuroinflammation in stroke.Lipopolysaccaride(LPS)is an endotoxin from the outer membrane of Gram-negative bacteria that activates microglia.MTT assay was used to observe the cell viability.The content of NO in supernatant was measured by Griess reagent.The levels of IL-1β,IL-6 and TNF-αin supernatant were detected by ELISA kits.The intracellular COX-2,TLR4,and My D88expression was assayed by Western blotting.RESULTS RC extract 30 and 100μg·m L-1significantly decreased the production of related inflammatory factors such as NO(P<0.05,P<0.01),IL-1β(P<0.01,P<0.01),IL-6(P<0.05,P<0.01)and TNF-α(P<0.01,P<0.01).Furthermore,RC extract significantly inhibited the COX-2,TLR4,and My D88 expression induced by LPS in BV2cells.CONCLUSION RC extract may have therapeutic potential for the improvement of neuroinflammation,and the mechanism may be involved in down-regulation of TLR4/My D88 inflammation pathway.
OBJECTIVE To investigate the effects of ex-tract of Ramulus Cinnamom (RC) against LPS-induced inflammation in microglia. METHODS Activated microglia releases various pro-inflammatory cytokines to induce neuroinflammation in stroke. Lipopolysaccaride (LPS) is an endotoxin from the outer membrane of Gram-negative bacteria that activates microglia. MTT assay was used to observe the cell viability. The content of NO in supernatant was measured by Griess reagent. The levels of IL-1β, IL-6 and TNF-αin supernatant were detected by ELISA kits The intracellular COX-2, TLR4, and My D88 expression was assayed by Western blotting .RESULTS RC extract 30 and 100 μg · m L -1 significantly reduced the production of related inflammatory factors such as NO (P <0.05, P <0.01), IL (P <0.01, P <0.01), IL-6 (P <0.05, P <0.01) and TNF-α , and My D88 expression induced by LPS in BV2 cells. CONCLUSION RC extract may have therapeutic potential for the improvemen t of neuroinflammation, and the mechanism may be involved in down-regulation of TLR4 / My D88 inflammation pathway.