首页> 外文期刊>American Journal of Clinical and Experimental Medicine >Effect of 'Nourishing Yin and Qi, Promoting Blood Circulation and Detoxification' on Endoplasmic Reticulum Stress CHOP Apoptotic Bypass in Diabetic Atherosclerosis
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Effect of 'Nourishing Yin and Qi, Promoting Blood Circulation and Detoxification' on Endoplasmic Reticulum Stress CHOP Apoptotic Bypass in Diabetic Atherosclerosis

机译:“滋阴益气,活血解毒”对糖尿病性动脉粥样硬化内质网应激CHOP凋亡旁路的影响

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To explore the mechanism of Huoxue Jiedu Jiangtang Recipe (HJJR) in alleviating endoplasmic reticulum stress (ERS) - inflammation, inhibiting ERS apoptotic bypass of CHOP and alleviating diabetic atherosclerosis (AS). Diabetic AS rats were duplicated by feeding of high lipid diet and intraperitoneal injection of streptozotocin. After diabetes modeled successfully, the rats were randomly divided into model group, low-dose HJJR group (HJJR_1), high-dose HJJR group (HJJR_2) and western medicine group (Gliquidone+ Benazepril), and accepted corresponding drugs for 2 months respectively. The same batch of rats were taken as normal control group and fed with common diet. The levels of glycosylated hemoglobin (GHb), blood lipid, fasting serum insulin (FINS) and insulin resistance index (IRI) were measured in each group. The contents of inflammatory factors TNF-α and IL-6 were detected by immunohistochemistry. The mRNA transcription of GRP78 and caspase-12 were tested by reverse- transcription polymerase chain reaction (RT-PCR). The apoptotic level of aortic cells was checked by TUNEL. Compared with the model group, all drug groups could significantly reduce GHb, IRI, TG and LDL-C (P0.05), increase FINS and HDL-C (P0.05), down-regulate transcription of CHOP and GRP78 (P0.05), reduce inflammatory factors TNF-a, IL-6, and decreased aortic apoptosis index (AI) (P0.05). Compared with the western medicine group, the effect of HJJR2 group was more significant (P0.05). HJJR could alleviate insulin resistance, correct lipid metabolism disorder, depress endoplasmic reticulum stress-induced inflammatory reaction, and inhibit endoplasmic reticulum stress-induced apoptotic bypass of CHOP in arterial cells. The therapeutic effect is dose dependent.
机译:探讨活血解毒降糖方(HJJR)减轻内质网应激(ERS)炎症,抑制CHOS ERS凋亡和减轻糖尿病性动脉粥样硬化(AS)的机制。通过高脂饮食和腹腔注射链脲佐菌素来复制糖尿病AS大鼠。糖尿病成功建模后,将大鼠随机分为模型组,低剂量HJJR_1组(HJJR_1),高剂量HJJR组(HJJR_2)和西药组(Gliquidone +贝那普利),分别接受相应药物治疗2个月。将同一批次的大鼠作为正常对照组并以普通饮食喂养。每组测量糖化血红蛋白(GHb),血脂,空腹血清胰岛素(FINS)和胰岛素抵抗指数(IRI)的水平。免疫组化法检测炎症因子TNF-α和IL-6的含量。通过逆转录聚合酶链反应(RT-PCR)测试了GRP78和caspase-12的mRNA转录。通过TUNEL检查主动脉细胞的凋亡水平。与模型组相比,所有药物组均可显着降低GHb,IRI,TG和LDL-C(P <0.05),增加FINS和HDL-C(P <0.05),下调CHOP和GRP78的转录(P < 0.05),降低炎症因子TNF-a,IL-6和降低主动脉凋亡指数(AI)(P <0.05)。与西药组相比,HJJR2组疗效更显着(P <0.05)。 HJJR可以减轻胰岛素抵抗,纠正脂质代谢紊乱,抑制内质网应激诱导的炎症反应,并抑制内质网应激诱导的CHOP凋亡。治疗效果是剂量依赖性的。

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