Z L Hu1, J P Zhang, X B Yu, W Lin, D H Qian, M B Wan. 1. Research Laboratory of Natural and Synthetic Drugs, College of Pharmacy, Second Military Medical University, Shanghai, China.
Abstract
AIM: To study the effects of matrine (Mat) on lipopolysaccharides (LPS)-induced fatal hepatitis in D-galactosamine (D-GalN)-sensitized mice and tumor necrosis factor (TNF) release from peritoneal macrophages (PMO). METHODS: Mice were pretreated with Mat (10, 50 mg.kg-1, i.p., bid x 3 d), and then injected i.p. LPS + D-GalN. Liver injury was assessed by quantifying plasma activity of alanine aminotransferase (ALT) and histopathological examination. The TNF activities in the supernatants of mouse PMO stimulated with LPS in the presence of Mat (32.5-500 mg.L-1) were monitored by the L929 target cells lytic assay. RESULTS: Mat pretreatment markedly diminished hepatic injury induced by LPS in combination with D-GalN. Mat inhibited LPS-induced TNF release from mouse PMO in vitro in a concentration-dependent manner. CONCLUSION: Mat protected the D-GalN-treated mice from the development of fatal hepatitis induced by LPS, and inhibited the LPS-induced TNF release from mouse PMO.
AIM: To study the effects of matrine (Mat) on lipopolysaccharides (LPS)-induced fatal hepatitis in D-galactosamine (D-GalN)-sensitized mice and tumor necrosis factor (TNF) release from peritoneal macrophages (PMO). METHODS:Mice were pretreated with Mat (10, 50 mg.kg-1, i.p., bid x 3 d), and then injected i.p. LPS + D-GalN. Liver injury was assessed by quantifying plasma activity of alanine aminotransferase (ALT) and histopathological examination. The TNF activities in the supernatants of mouse PMO stimulated with LPS in the presence of Mat (32.5-500 mg.L-1) were monitored by the L929 target cells lytic assay. RESULTS:Mat pretreatment markedly diminished hepatic injury induced by LPS in combination with D-GalN. Mat inhibited LPS-induced TNF release from mouse PMO in vitro in a concentration-dependent manner. CONCLUSION:Mat protected the D-GalN-treated mice from the development of fatal hepatitis induced by LPS, and inhibited the LPS-induced TNF release from mouse PMO.