目的:研究红景天苷(salidroside,SAL)对肥胖小鼠胰腺脂质沉积及磷脂酰肌醇-3-激酶(phosphatidylinositol 3-kinase,PI3K)/Akt信号的影响。方法:采用高脂饲料喂养法(high-fat diet,HFD)建立肥胖小鼠模型,随机分为模型组和SAL(100 mg·kg^-1·d^-1)治疗组,同时设立正常对照组,连续给药8周;治疗期间检测体质量与血糖变化,治疗结束后解剖小鼠,收集胰腺组织行HE染色病理切片制作,以生化分析法对胰腺组织中甘油三酯(triglyceride,TG)含量进行检测,以Western blot法对胰腺组织PI3K/Akt信号水平进行检测。结果:SAL治疗可缓解HFD引起的体质量增加和血糖升高,病理切片和TG含量检测结果显示SAL可减少胰腺组织的异位脂肪沉积,Western blot结果提示SAL可增加胰腺组织PI3K/Akt信号的关键分子Akt和糖原合成酶激酶β的磷酸化水平。结论:SAL干预可减少HFD肥胖小鼠胰腺组织脂质沉积,并激活胰腺PI3K/Akt信号。
Objective To study the effects of salidroside(SAL) on pancreatic lipid deposition and phosphatidylinositol 3-kinase(PI3 K)/Akt signal in obese mice. Methods Obese mouse models were established by high-fat diet(HFD) and randomly divided into model group and SAL(100 mg·kg^-1·d^-1) treatment group, and normal control group was established at the same time. The drug was given for 8 weeks. The body mass and blood glucose were measured during the treatment. The mice were dissected after the treatment, and the pancreatic tissue was collected and stained with HE staining. The content of triglyceride(TG) in pancreatic tissue was detected by biochemical analysis. The PI3 K/Akt signal level of pancreatic tissue was detected by Western blot. Results SAL treatment can alleviate the increase in body mass and blood glucose caused by HFD. The results of pathological section and TG content showed that SAL can reduce ectopic fat deposition in pancreatic tissue. Western blot results suggested that SAL can increase the phosphorylation levels of Akt and glycogen synthase kinase β, key molecules of PI3 K/Akt signal in pancreatic tissue. Conclusion SAL intervention can reduce pancreatic lipid deposition and activate pancreatic PI3 K/Akt signal in HFD-induced obese mice.
Journal of Hubei University of Medicine