摘要
目的观察黄芪多糖(astragalus polysaccharides,APS)对糖尿病(diabetes mellitus,DM)仓鼠糖脂代谢和过氧化物酶体增生物激活体-α(proxisome proliferator activated receptors-α,PPAR-α)及其下游基因表达的影响,探讨其对DM心肌病变可能的干预机制。方法45只仓鼠随机分为3组。正常对照组:健康仓鼠15只;DM组:链脲佐菌素(STZ)诱导糖尿病仓鼠15只;APS治疗组:STZ诱导糖尿病仓鼠15只,每天给予APS2g/kg,灌胃10周。分别检测3组仓鼠的血糖、血脂、胰岛素、C肽、心肌酶谱水平,心肌细胞超微结构,荧光定量RT-PCR法和Western blot法分别检测心肌PPAR-α及靶基因(FATP、ACS)mRNA和蛋白的表达。结果DM组与正常组比较有明显的脂代谢紊乱;APS治疗组血糖、糖化血清蛋白、心肌酶谱和血脂水平较DM组明显下降,胰岛素和C肽水平无差异;APS治疗组心肌超微结构异常较DM组明显改善;APS组心肌组织PPAR-α、FATP和ACS的基因及蛋白表达较DM组显著增高。结论APS可以通过影响PPAR-α表达部分改善糖尿病仓鼠心肌脂代谢紊乱。
Objective This article was designed to observe the effects of astragalus polysaccharides (APS) on glucose and lipid metabolism, and on expressions of proxisome proliferator activated receptors-α (PPAR-α) and its downstream genes in diabetic hamsters cardiomyopathy. Methods Forty-five hamsters were divided into 3 groups randomly: normal control group (15 normal hamsters), diabetic control group [15 streptozotocin (STZ)-induced diabetic hamsters], and astragalus polysaccharides (APS)-therapy group (15 STZ-induced diabetic hamsters administered with APS 2 g/kg per day orally for 10 weeks). The levels of insulin, C-peptide, myocardial enzymes, glycosylated serum protein (GSP) and lipoprotein of all hamsters were measured. The ultrastructure of myocardium was studied, and the gene and protein expressions of PPAR-α, FATP and ACS were also detected by fluorescent quantitative RT-PCR and Western blot. Results It was shown that Compared with DM group, the levels of GSP, myocardial enzymes and lipoprotein of hamsters in APS-therapy group were lower, the myocardial ultrastructure of hamsters in APS-therapy group was well-protected, and the gene and protein expression of PPAR-α, FATP and ACS of hamsters in APS-therapy group were higher. Conclusions APS is partly effective in treating diabetic cardiomyopathy.
出处
《复旦学报(医学版)》
CAS
CSCD
北大核心
2010年第2期194-197,215,共5页
Fudan University Journal of Medical Sciences
基金
上海市科学委员会科研计划项目(05ZR14024)
关键词
黄芪多糖
糖尿病
心肌病变
超微结构
过氧化物酶体增生物激活体-α
astragalus polysaccharide
diabetes mellitus
cardiomyopathy
ultrastructure
proxisome proliferator activated receptors-α