Protective Effects and Mechanisms of Polygonatum kingianum on Nonalcoholic Fatty Liver in Rats / 中国药学杂志

ABSTRACT

OBJECTIVE: To investgate the protective effects and mechanisms of Polygonatum kingianum on nonalcoholic fatty liver induced by high-fat diet in rats. METHODS: A total of 42 rats were randomly divided into normal control group (normal saline), model group (normal saline), resveratrol group (positive control, 40 mg•kg-1) and low-, middle-and high-dose P. kingianum group (1, 4, 8 g•kg-1). They were intragastrically given corresponding compounds (or normal saline) once a day, lasting for 14 weeks. Nonalcoholic fatty liver was induced by feed with high-fat diet for 14 weeks in those groups except for normal control group. Blood was taken from the corneas at 0, 6, 12 and 14 week, and then the levels of triglyceride (TG) and total cholesterol (TC) in serum were determined. Afterword, the rats were sacrificed at 14 week followed by the measurement of organs indices of liver, spleen and kidney, as well as the detection of levels of TC, TG, high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) in liver tissues. Furthermore, the levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), ATP synthase and respiratory chain complex and Ⅱ in hepatic mitochondria were determined. RESULTS: Nonalcoholic fatty liver was successfully induced by high-fat diet in rats. The different doses of water extract of P. kingianum could significantly inhibit the increasing of liver index and serum TC in high-fat diet-induced rats, alleviate swelling, degeneration, necrosis and inflammatory injury of hepatic cells, inhibit the increasing of TC, TG and LDL-C and decrease of HDL-C in liver tissues, as well as inhibit the exaltation of MDA level and reduction of SOD, GSH-PX, ATP synthase and respiratory chain complex and Ⅱ activity in hepatic mitochondria. CONCLUSION: P. kingianum shows protective effects on high-fat diet-induced nonalcoholic fatty liver in rats. The action mechanism may be related to the elimination of oxidative stress product (MDA) and improvement of antioxidant enzyme activity (SOD and GSH-PX) in hepatic mitochondria, as well as the improvement of energy metabolism obstacle.