穴位埋线对非酒精性脂肪性肝病大鼠SREBP-1表达的影响

摘要

Objective:To investigate the effect of point embedding therapy on expression of sterol regulatory element binding protein-1 (SREBP-1)in rats with nonalcoholic fatty liver disease (NAFLD). Methods:40 wistar rats were randomly divided into the normal control group,the model group,the point embedding therapy for 4 weeks group and the point embedding therapy for 8 weeks group. After the NAFLD animal model duplicated with high fat diet,the point embedding therapy were used in the corresponding groups. After 10 weeks,some indices were detected in the serum such as ALT,AST,TG and TC. The pathological changes of the liver were also observed. The expression of SREBP-1 was detected by the Western blot method. Results:Compared with the normal control group,the serum ALT,AST,TG,TC and the hepatic TG,TC in model group were markedly higher.The model group presented with steatosis,inflammation or inflammation necrosis. Meanwhile,the ALT,AST,TG,TC and liver tissue TG,TC were increased significantly. Above indices in the point embedding therapy group were decreased. The fatty degeneration and the inflammation necrosis degree were reduced in this group. Expressions of SREBP-1 in the model group were more remarkably than those in the normal group. Nevertheless,these expressions of the point embedding therapy group were fewer significantly than those of the model group.Conclusion: Point embedding therapy has the protective effects against NAFLD in rats induced by high fat diet possibly through its regulating the lipid metabolism and inhibiting the expression of SREBP-1.%目的 探讨穴位埋线对大鼠非酒精性脂肪性肝病(NAFLD)及其胆固醇调控元件结合蛋白-1(SREBP-1)的影响.方法 雄性wistar大鼠40只,随机分为正常对照组、模型组、穴位埋线4周组、穴位埋线8周组,每组各10只.应用高脂饮食复制大鼠NAFLD模型.穴位埋线治疗组大鼠在进行高脂饮食同时每日给予穴位埋线干预治疗.治疗10周后,检测血清丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、甘油三酯(TG)、总胆固醇(TC)和肝组织TG、TC,并观察肝脏的病理改变;Western B1ot法检测肝脏SREBP-1表达.结果 与正常对照组相比,模型组大鼠病理显示脂肪变性、炎症或炎症坏死并伴有血清ALT、AST、TG、TC及肝组织TG、TC明显升高.穴位埋线组大鼠血清ALT、AST、TG、TC和肝组织TG、TC降低,且肝脏脂肪变性和炎症坏死程度减轻.模型组SREBP-1的表达明显高于正常组,穴位埋线组SREBP-1的表达较模型组明显减少.结论 穴位埋线对大鼠高脂饮食诱导的NAFLD有防治作用,其机制可能与调节脂质代谢、抑制氧化过程,推测与抑制SREBP-l表达有关.