摘要
目的:观察红景天苷(salidroside,SDS)对大鼠非酒精性脂肪性肝炎(NASH)肝组织氧化应激的影响。方法:以高脂高胆固醇饮食14周诱导建立大鼠NASH模型,药物干预组在造模第8周末时给予SDS 300 mg·kg-1·d-1体重灌胃连续6周,在14周末检测大鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆固醇(TC)和甘油三酯(TG),以及肝组织TC、TG、丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽(GSH)含量的变化,ELISA检测8-异前列腺素F2α(8-iso-PGF2α)的水平变化,HE染色观察肝组织病理学变化,免疫组化观察8-羟基脱氧鸟苷酸(8-OHdG)表达的变化。结果:在14周末,NASH模型组大鼠肝组织病理学检查显示肝组织呈中重度脂肪变性并同时伴有炎症细胞浸润;与正常对照组相比,NASH模型组大鼠血清ALT、AST、TG和TC,以及肝TG、TC和MDA的含量显著上升,而肝SOD和GSH的含量显著下降,8-iso-PGF2α的水平显著上升,免疫组化显示8-OHdG表达的阳性细胞数显著增多。与模型组相比,SDS药物干预组大鼠ALT、AST、TG、TC、MDA和8-iso-PGF2α的含量均显著下降,而肝SOD和GSH的含量显著上升,肝病理学变化得到显著改善,8-OHdG表达的阳性细胞数明显减少。结论:SDS对高脂高胆固醇饮食诱导的NASH有较好的抑制效果,其机制可能与SDS的抗氧化作用有关。
AIM：To explore the effects of salidroside （SDS） on the oxidative stress in liver tissues from rats with non-alcoholic steatohepatitis （NASH）. METHODS：The experimental animal model of NASH was established in SD rats fed on high-fat and high-cholesterol diet （HFHCD） for 14 weeks. SDS （300 mg·kg^-1·d^-1） was administered via gavage daily from the 8th week after HFHCD feeding. At the end of the 14th week, serum samples were taken for detection of alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, triglyceride （TG） and total cholesterol （TC）. Liver tissues were taken for TG, TC, malondialdehyde （MDA）, superoxide dismutase （SOD） and glutathione （GSH） detection. The content of 8-isoprostaglandin F2α （8-iso-PGF2α） in liver tissues was determined by ELISA. The liver histopathological changes were observed under microscope with HE staining. The expression of 8-hydroxydeoxyguanosine （8-OHdG） in liver tissues was determined by immunohistochemical staining. RESULTS：At the end of the 14th week, ALT, AST, TG and TC in serum, and TG, TC, MDA and 8-iso-PGF2α in liver homogenate in NASH model group were significantly increased compared with control group, while SOD and GSH in liver tissues were significantly decreased. The liver expression of 8-OHdG in NASH model group was higher than that in control group. Compared with NASH model group, SDS significantly inhibited the elevation of serum ALT, AST, TG and TC, and liver TG, TC, MDA and 8-iso-PGF2α, but increased the levels of SOD and GSH in liver tissues. Meanwhile, the liver histopathological score and 8-OHdG expression were decreased in SDS treatment group. CONCLUSION：Salidroside can effectively inhibit steatohepatitis induced by HFHCD, and its antioxidant effect may be one of the mechanisms.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2013年第9期1704-1708,共5页
Chinese Journal of Pathophysiology
