Protective effect of the extract of Terminalia catappa leaves on acute liver injury induced by D-GalN in mice.
- Author:
Xin-hui TANG
1
;
Jing GAO
;
Huan DOU
;
Yan-ping WANG
;
Li-zhi XU
;
Zeng-rong ZHU
;
Qiang XU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cells, Cultured; Chemical and Drug Induced Liver Injury; blood; etiology; pathology; Drugs, Chinese Herbal; isolation & purification; pharmacology; Female; Galactosamine; Liver; metabolism; pathology; Male; Mice; Mice, Inbred ICR; Plant Leaves; chemistry; Plants, Medicinal; chemistry; Pregnancy; Protective Agents; pharmacology; Terminalia; chemistry
- From: China Journal of Chinese Materia Medica 2004;29(11):1069-1073
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the hepatoprotective effect of the extract of Terminala catappa leaves (TCE) and the possible mechanisms underlying its protection on acute liver injury induced by D-Galactosamine (D-GalN).
METHODIn vivo: D-GalN-induced liver injury model was used to evaluate the effect of TCE on the activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in mice. Structure of liver was observed and liver mitochondrial swelling was measured following D-GalN injection without or with TCE. In vitro: D-GalN-induced primary cultured hepatocytes injury model was used to value the effect of TCE on cultured hepatocytes. Cell viability was measured by means of MTT assay, and the AST and superoxide dismutase (SOD) activities in supernatant of cultured cells were investigated also.
RESULTIn acute hepatic injury test, with oral pretreatment of TCE, remarkable rises in serum AST and ALT activities (2.95 fold and 3.35 fold) induced by D-GalN were obviously reversed and significant morphological changes were remarkably lessened. In addition, the decrease in sensitivity of mitochondrial swelling to the exotic Ca2+ stimulation induced by D-GalN was also prevented by TCE. In primary cultured hepatocytes of mice, it was found that incubation with TCE could prevent the decrease in cell viability in a dose-dependent manner. It was also found that both the increase in AST level (1.9 fold) and the decrease in SOD activity (48.0%) in supernatant of primary cultured hepatocytes induced by D-GalN could be inhibited by pretreatment of TCE.
CONCLUSIONTCE has hepatoprotective activity and the mechanisms underlying its protective effect may be related to its antioxidant activity and protection on both hepatocytes and liver mitochondria.