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电针对高脂饮食诱导的胰岛素抵抗大鼠内皮功能障碍的缓解作用及其对 PI3K/Akt 信号通路的影响。

Electroacupuncture mitigates endothelial dysfunction via effects on the PI3K/Akt signalling pathway in high fat diet-induced insulin-resistant rats.

机构信息

Department of Acupuncture and Moxibustion, Foshan Hospital of TCM, Foshan, Guangdong, China.

Clinical Medical College of Acupuncture and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, China.

出版信息

Acupunct Med. 2018 Jun;36(3):162-169. doi: 10.1136/acupmed-2016-011253. Epub 2018 Mar 3.

Abstract

OBJECTIVE

To investigate the effect of electroacupuncture (EA) on endothelial dysfunction related to high fat diet (HFD)-induced insulin resistance through the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) signalling pathway.

METHODS

Twenty-four male Sprague-Dawley rats were fed a regular diet (Control group, n=8) or a HFD (n=16) for 12 weeks to induce an insulin resistance model. HFD-fed rats were divided into two groups that remained untreated (HFD group, n=8) or received electroacupuncture (HFD+EA group, n=8). EA was applied at PC6, ST36, SP6 and BL23. At the end of the experiment, fasting blood glucose (FBG), serum insulin (FINS), serum C-peptide (C-P) and homeostatic model assessment of insulin resistance (HOMA-IR) indices were determined. Pancreatic islet samples were subjected to histopathological examination. The thoracic aorta was immunostained with anti-rat insulin receptor substrate (IRS)-1, Akt and endothelial nitric oxide synthase (eNOS) antibodies. mRNA and protein expression of IRS-1, PI3K, Akt2 and eNOS in the vascular endothelium were determined by real-time PCR and Western blot analysis, respectively.

RESULTS

The bodyweight increase of the HFD+EA group was smaller than that of the untreated HFD group. Compared with the HFD group, the levels of FBG, FINS, C-P and HOMA-IR in the HFD+EA group decreased significantly (P<0.01). Histopathological evaluation indicated that EA improved pancreatic islet inflammation. The expression of endothelial markers, such as IRS-1, PI3K, Akt2 and eNOS, decreased in the HFD group, while EA treatment appeared to ameliorate the negative impact of diet.

CONCLUSION

EA may improve insulin resistance and attenuate endothelial dysfunction, and therefore could play a potential role in the prevention or treatment of diabetic complications and cardiovascular disease through the PI3K/Akt signalling pathway.

摘要

目的

通过磷脂酰肌醇 3-激酶(PI3K)-蛋白激酶 B(Akt)信号通路研究电针对高脂饮食(HFD)诱导的胰岛素抵抗相关内皮功能障碍的影响。

方法

将 24 只雄性 Sprague-Dawley 大鼠分别喂饲普通饮食(对照组,n=8)或 HFD(n=16)12 周,以诱导胰岛素抵抗模型。HFD 喂养的大鼠分为两组,一组未治疗(HFD 组,n=8),另一组给予电针治疗(HFD+EA 组,n=8)。电针治疗选穴 PC6、ST36、SP6 和 BL23。实验结束时,测定空腹血糖(FBG)、血清胰岛素(FINS)、血清 C 肽(C-P)和稳态模型评估的胰岛素抵抗指数(HOMA-IR)。对胰腺胰岛进行组织病理学检查。用抗大鼠胰岛素受体底物(IRS)-1、Akt 和内皮型一氧化氮合酶(eNOS)抗体对胸主动脉进行免疫染色。用实时 PCR 和 Western blot 分析分别测定血管内皮 IRS-1、PI3K、Akt2 和 eNOS 的 mRNA 和蛋白表达。

结果

HFD+EA 组的体重增加小于未治疗的 HFD 组。与 HFD 组相比,HFD+EA 组的 FBG、FINS、C-P 和 HOMA-IR 水平显著降低(P<0.01)。组织病理学评价表明电针治疗改善了胰岛炎症。HFD 组内皮标志物 IRS-1、PI3K、Akt2 和 eNOS 的表达降低,而电针治疗似乎改善了饮食的负面影响。

结论

电针可能通过 PI3K/Akt 信号通路改善胰岛素抵抗和减轻内皮功能障碍,从而在预防或治疗糖尿病并发症和心血管疾病方面发挥潜在作用。

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