Anti-inflammation effect of the extract of a Zhuang medicine Ventilago leiocarpa and its related mechanism
Objective To determine the anti-inflammation effect and mechanism of the extract of a Zhuang medicine Ventilago leiocarpa.Methods The mouse inflammation model was established by ear swelling induced by xylene,cotton ball granuloma,and peritoneal capillary permeability induced by glacial acetic acid.The mice were divided into a blank group,a dexamethasone positive control group(5 mg·kg-1),and high-,medium-and low-dose extract groups(8.0,4.0,and 2.0 g·kg-1).The mouse model of acute lung injury(ALI)induced by lipopolysaccharide(LPS)was established.The groups were the same as the above,and another model group was set up.The mice in each group were given corresponding medicine intragastrically once daily for 7 consecutive days.One hour after the last administration,the mice in the model group and each medicine group were intraperitoneally injected LPS(10 mg·kg-1)to replicate the mouse ALI model.Twenty-four hours after the intraperitoneal injection,the contents of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),and nuclear factor-KB(NF-KB)in the serum were detected by enzyme-linked immunosorbent assay.The content of TNF-α in the lung tissue and lung coefficient were measured.Results Compared with the blank group,the degree of ear swelling and the quality of cotton ball granuloma induced by xylene in the mice was decreased(P＜0.05,P＜0.01),and the peritoneal capillary permeability induced by glacial acetic acid of mice was significantly decreased(P＜0.05,P＜0.01)in each dose group.Compared with the model group,the contents of TNF-α,IL-1β,and NF-KB in the serum,the lung coefficient and the contents of TNF-α in the lung tissue were significantly decreased(P＜0.05,P＜0.01)in each dose group.Conclusion The extract of Ventilago leiocarpa has significant anti-inflammation effect on three inflammation mouse models.Its anti-inflammation mechanism may be associated with decreasing the contents of TNF-α,IL-1β,and NF-KB,regulates NF-κB inflammatory signaling pathway,and inhibit inflammation reaction.
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