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OBJECTIVE To investigate toll-like receptor 4(TLR4)-related the regulation of Ornithog-alum caudatum extract(OCE)on inflammatory responses in lipopolysaccharide(LPS)activated macro-phages.METHODS Primary peritoneal macrophage,Raw 264.7,and THP-1 were incubated in 96-well plate for 24 h and treated with OCE of the concentration of 0-400 μg/ml for 4h.The viability of cells was measured by MTT assay.Specific concentrations of OCE were added into the medium of primary peri-toneal macrophage, Raw 264.7, and THP-1, respectively, then following with lipopolysaccharides (LPS). Cells were harvested and the total cellular protein and nuclear protein were extracted, and the protein content was determined using BCA protein assay Kit.The expressions of TLR4,inducible nitric oxide synthase(iNOS),cyclooxygenase 2(COX-2),α-inhibitor of NF-κB(IκB-α)and nuclear factor-κB (NF-κB)were assayed by Western blot.The expressions of interleukin-1α(IL-1α),interleukin-1β(IL-1β), interleukin-18(IL-18),and tumor necrosis factor-α(TNF-α)were measured by RT-PCR.RESULTS The results of MTT showed that OCE has no cytotoxicity in Raw 264.7 cells between 1.56 μg/ml and 400 μg/ml. Compared with normal group,the expressions of TLR4,iNOS,COX-2,NF-κB and IL-1α,IL-1β,IL-18, TNF-α,the level of nitric oxide(NO)were significantly increased by LPS stimulation,while OCE pretreat-ment reduced these increase induced by LPS. However, OCE pretreatment reversed the reduction of IκB-α after LPS stimulation.CONCLUSION OCE might suppress TLR4 expression and block the inflamma-tion process of NF-κB and iNOS,further decrease the expression of COX-2 and inhibit the release of inflammatory factors.
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Rat models of liver fibrosis were made by carbon tetrachloride, and the serum levels of AST, ALT, γ-GT, MDA, GSH-px, SOD were detected, serum markers of PCⅢ, IV-C, LN, HA were detected by ELISA method. HE and Masson staining were conducted in hepatic tissues to observe pathological variations. Collagen Ⅲ, TGF-β, α-SMA, E-cadherin were detected by Western blot. The curative effect of the extract of Ornithogalum caudatum on rat liver fibrosis induced by CCl4was observed and the mechanism was discussed. The experiment results showed that the extract of O. caudatum (50, 150, 500 mg•kg⁻¹) obviously decreased the serum levels of AST, ALT, γ-GT, MDA, increased the serum levels of GSH-px, SOD, decreased the expression of serum markers of PCⅢ, IV-C, LN, HA, and improved the liver pathological variations of fibrotic rats. The experiment proved that the extract of O. caudatum could treat the liver fibrogenesis induced by CCl4 in rats. The positive medicine may inhibit accumulation of extracellular and activate hepatic stellate cell and epithelial-mesenchymal transition.
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Objective: To investigate the antitumor, analgesic, and anti-inflammatory effects of Ornithogalum caudatum extract (OCE). Methods: The MFC, HepG-2, and S180 tumor-bearing mice models were established, and the tumor inhibitory rate of OCE was calculated; The analgesic effect of OCE was observed by acetic acid writhing test of mice; The anti-inflammatory effect of OCE was observed in xylene-induced ear edema model of mice. Results: OCE (5.0 and 2.5 g/kg) could effectively inhibit the growth of solid tumors in tumor-bearing mice in a dose-dependent manner (P < 0.05, 0.001); Compared with the model group, OCE (5.0 and 2.5 g/kg) could significantly inhibit the writhing response (P < 0.05, 0.001) and xylene-induced ear edama (P < 0.05, 0.01). Conclusion: OCE has certain antitumor, analgesic, and anti-inflammatory effects, suggesting they may be worth further investigation.