X H Chen1, Y M Hu, Y Q Liao. 1. Department of Pharmacology, Third Military Medical College, Chongqing, China.
Abstract
AIM: To study the protective effects of tetrandrine (Tet) on CCl4-injured hepatocytes. METHODS: The cultured rat liver cells were poisoned by CCl4 (10 mmol.L-1). The membrane fluidity was detected by 1,6-diphenyl-1,3,5-hexatriene (DPH), a lipid probe. The Ca2+ concentration was assayed with Fura 2-AM, a sensitive calcium indicator. RESULTS: Tet (1-1000 nmol.L-1) increased viability of liver cell (from 71% to 72%-89%), reduced lactate dehydrogenase (LDH) release, and malondialdehyde (MDA) formation. Tet prevented the heightening of the intracellular Ca2+ concentration and the attenuation of the membrane fluidity of liver cells (P < 0.05). CONCLUSION: Tet had a protective effect on CCl4-injured hepatocytes by inhibiting the lipid peroxidation, improving the membrane fluidity, and lessening the Ca2+ concentration.
AIM: To study the protective effects of tetrandrine (Tet) on CCl4-injured hepatocytes. METHODS: The cultured rat liver cells were poisoned by CCl4 (10 mmol.L-1). The membrane fluidity was detected by 1,6-diphenyl-1,3,5-hexatriene (DPH), a lipid probe. The Ca2+ concentration was assayed with Fura 2-AM, a sensitive calcium indicator. RESULTS:Tet (1-1000 nmol.L-1) increased viability of liver cell (from 71% to 72%-89%), reduced lactate dehydrogenase (LDH) release, and malondialdehyde (MDA) formation. Tet prevented the heightening of the intracellular Ca2+ concentration and the attenuation of the membrane fluidity of liver cells (P < 0.05). CONCLUSION:Tet had a protective effect on CCl4-injured hepatocytes by inhibiting the lipid peroxidation, improving the membrane fluidity, and lessening the Ca2+ concentration.