论文部分内容阅读
目的:观察肝脾肾同调的组方降糖消渴颗粒对糖尿病(DM)大鼠脂代谢的作用,并通过其对腺苷酸活化蛋白激酶(AMPK)信号通路的影响探讨可能的作用机制。方法:SD大鼠高脂饲料喂养4周后结合腹腔注射链脲佐菌素(STZ)30mg/kg,建立2型DM大鼠模型,将成模的大鼠按血糖随机分为模型组、阳性对照组(吡格列酮片1.5mg/kg体质量)、降糖消渴颗粒组(9.0g生药/kg体质量),并设正常对照组。干预4周后,称量大鼠肝重,检测大鼠血清血脂4项总胆固醇(TC),甘油三酯(TG),低密度脂蛋白胆固醇(LDL-C),高密度脂蛋白胆固醇(HDL-C)水平及肝功能相关指标,实时荧光定量PCR法检测大鼠肝脏组织AMPKαm RNA表达,以及AMPKα、p-AMPKα、乙酰辅酶A羧化酶(p-ACC)蛋白表达,观察降糖消渴颗粒对上述指标的影响。结果:降糖消渴颗粒能够使DM大鼠血清TC、TG、LDL-C水平显著下降33%、57%、44%,同时使HDL-C水平显著提高,ALT水平显著降低,与模型组比较,差异具有统计学意义(P<0.05,P<0.01)。与模型组相比,降糖消渴颗粒能显著上调DM大鼠肝脏AMPKαm RNA及蛋白表达,同时提高DM大鼠骨肝脏AMPKα、p-AMPKα及p-ACC蛋白表达量(P<0.05)。结论:降糖消渴颗粒能改善DM大鼠脂代谢,其作用机制可能与调节肝脏AMPK信号通路相有关。
OBJECTIVE: To observe the effect of HGPTD on lipid metabolism in diabetic rats and to explore its possible mechanism through its effect on AMPK signal pathway. Methods: SD rats were fed with high-fat diet for 4 weeks and peritoneally injected with streptozotocin (STZ) 30mg / kg to establish type 2 DM model. The rats were randomly divided into model group and control group (Pioglitazone tablets 1.5mg / kg body weight), hypoglycemic diabetes group (9.0g crude drug / kg body weight), and set the normal control group. Four weeks after the intervention, the rats were weighed, and the levels of serum TC, TG, LDL-C, HDL C) and liver function were measured. The expression of AMPKαmRNA and the protein expressions of AMPKα, p-AMPKα and p-ACC in liver were detected by real-time fluorescence quantitative PCR. The impact of particles on these indicators. Results: Jiangtangxieke granule could significantly decrease the levels of TC, TG and LDL-C in DM rats by 33%, 57% and 44%, and at the same time, the levels of HDL-C and ALT were significantly decreased , The difference was statistically significant (P <0.05, P <0.01). Compared with the model group, Jiangtangxiaoke Granule could significantly upregulate AMPKαmRNA and protein expression in DM rats liver and increase the expression of AMPKα, p-AMPKα and p-ACC protein (P <0.05). Conclusion: Jiangtangxieke Granule can improve lipid metabolism in DM rats, and its mechanism may be related to regulation of hepatic AMPK signaling pathway.