Chang Shan-Shan, Zhou Dan, Meng Guo-Liang, Wu Feng, Wang Shuang, Chen Xiao, Xu Ji-Liang
Department of Pharmacology, Medical School of Nantong University, Nantong 226001, China.
Zhongguo Zhong Yao Za Zhi. 2012 Oct;37(20):3102-6.
To study the effect of Ganoderma lucidum polysaccharides on oxidative stress of hyperlipidemic fatty liver in rats.
Seventy-two SD rats were randomly divided into six groups, namely the normal control group (NG), the model group (MG), the G. lucidum polysaccharides groups of low, middle and high dose (GLPs-LG, GLPs-MG, GLPs-HG) and the Simvastatin group (SV). The rats were fed with high fat diet to establish the model of hyperlipidemic fatty liver in rats. After administration for 12 weeks, rats in each group were tested with the following indexes: total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol (LDL-C), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) in serum as well as the contents of SOD, MDA, GSH-Px and T-AOC in hepatic tissues. Histopathological changes of hepatic tissues were observed under light glass.
The contents of TC, TG and LDL-C were significantly increased in the model group (P < 0.01). Compared with the model group, both the GLPs-M group and the GLPs-H group showed significant decreases in TC, TG and LDL-C (P < 0.05 or P < 0.01), while the GLPs-H group showed a notable increase in HDL-C (P < 0.05). Compared with the model group, both the GLPs-M group and the GLPs-H group showed significant decreases in MDA (P < 0.05 or P < 0.01) and notable increases in SOD, GSH-Px, T-AOC (P < 0.05 or P < 0.01). The GLPs-M group and the GLPs-H group proved a remarkable alleviation in fatty degeneration of hepatic cells.
G. lucidum polysaccharides can significantly reduce the blood fat level of hyperlipidemic fatty liver in rats and effectively inhibit oxidant stress, showing the effect on preventing and treating hyperlipidemic fatty liver in rats to some extent.
研究灵芝多糖对高脂血症性脂肪肝大鼠氧化应激的影响。
将72只SD大鼠随机分为6组，即正常对照组（NG）、模型组（MG）、低、中、高剂量灵芝多糖组（GLPs-LG、GLPs-MG、GLPs-HG）和辛伐他汀组（SV）。采用高脂饮食喂养大鼠建立高脂血症性脂肪肝模型。给药12周后，检测各组大鼠血清总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、总抗氧化能力（T-AOC）以及肝组织中SOD、MDA、GSH-Px、T-AOC的含量。在光学显微镜下观察肝组织的病理变化。
模型组大鼠TC、TG和LDL-C含量显著升高（P<0.01）。与模型组相比，GLPs-M组和GLPs-H组大鼠的TC、TG和LDL-C均显著降低（P<0.05或P<0.01），而GLPs-H组大鼠的HDL-C显著升高（P<0.05）。与模型组相比，GLPs-M组和GLPs-H组大鼠的MDA均显著降低（P<0.05或P<0.01），SOD、GSH-Px、T-AOC均显著升高（P<0.05或P<0.01）。GLPs-M组和GLPs-H组大鼠肝细胞脂肪变性明显减轻。
灵芝多糖可显著降低高脂血症性脂肪肝大鼠的血脂水平，有效抑制氧化应激，在一定程度上显示出对大鼠高脂血症性脂肪肝的防治作用。
