發(fā)布時間：2018-03-31 23:24

  本文選題：GW　切入點：高糖　出處：《中國藥理學通報》2015年12期

【摘要】：目的探討GW0742對高糖損傷大鼠胸主動脈內(nèi)皮的作用及可能機制。方法葡萄糖55 mmol·L~(-1)(high glucose,HG)孵育大鼠胸主動脈,以乙酰膽堿(acetylcholine,ACh)誘導的內(nèi)皮依賴性舒張作用為內(nèi)皮功能完整性指標,HE染色觀察血管形態(tài)結(jié)構(gòu)變化,硝酸還原法測量血管內(nèi)一氧化氮(nitric oxide,NO)含量,利用q RT-PCR和Western blot方法檢測血管中過氧化物酶增殖物激活受體β(peroxisome proliferator-activated receptorβ,PPARβ)、核轉(zhuǎn)錄因子κB(nuclear transcription factor-κB,NF-κB)及內(nèi)皮型一氧化氮合酶(endothelial nitric oxide synthase,e NOS)m RNA和蛋白表達。結(jié)果 HG條件下,ACh的內(nèi)皮依賴性舒張作用明顯減弱(P0.01),內(nèi)皮功能受損;血管內(nèi)皮細胞和平滑肌細胞結(jié)構(gòu)完整性也被破壞;同時,PPARβm RNA和蛋白表達明顯降低(P0.01),而NF-κB p65的表達則升高(P0.01),e NOS的表達下降(P0.01),血管內(nèi)NO含量亦減少(P0.01);GW0742(0.01、0.1、1μmol·L~(~(-1)))能劑量依賴性地改善高糖損傷的ACh內(nèi)皮依賴性舒張作用(P0.01),減輕內(nèi)皮細胞和平滑肌細胞的損傷,上調(diào)PPARβ表達,減少NF-κB p65的表達,增加e NOS表達和NO的濃度(P0.01)。結(jié)論 GW0742對高糖損傷的大鼠胸主動脈內(nèi)皮有保護作用,該作用可能與其激活PPARβ,下調(diào)NF-κB,改善e NOSNO系統(tǒng)有關(guān)。
[Abstract]:Objective to investigate the effect of GW0742 on the endothelium of thoracic aorta of rats with high glucose injury and its possible mechanism. Methods the thoracic aorta of rats was incubated with glucose 55 mmol L~(-1)(high glucose. The endothelium-dependent relaxation induced by acetylcholine acetylcholine acetylcholine (ache) was used as an index of endothelial functional integrity to observe the changes of vascular morphology and structure by HE staining, and the nitric oxide nitric oxide (no) content in blood vessels was measured by nitric acid reduction method. Q RT-PCR and Western blot were used to detect the expression of peroxisome proliferator-activated receptor 尾 PPAR 尾, nuclear transcription factor B(nuclear transcription factor- 魏 B, endothelial nitric oxide synthase NOS)m RNA and protein in blood vessels. The dependent diastolic effect was significantly decreased, and the endothelial function was impaired. The structural integrity of vascular endothelial cells and smooth muscle cells was also destroyed. At the same time, the expression of PPAR 尾 m RNA and protein decreased significantly, while the expression of NF- 魏 B p65 increased and the expression of P0.01e NOS decreased. The content of no in blood vessel also decreased P0.01GW0742C0.01 渭 mol L-1). It can improve the endothelium-dependent relaxation effect of ACh induced by high glucose injury in a dose-dependent manner and alleviate the endothelium-dependent relaxation effect of P0.01. Damage to cells and smooth muscle cells, The expression of PPAR 尾 was up-regulated, the expression of NF- 魏 B p65 was decreased, the expression of e NOS and the concentration of no were increased. Conclusion GW0742 has protective effect on thoracic aorta endothelium in rats with high glucose injury, which may be related to its activation of PPAR 尾, down-regulation of NF- 魏 B and improvement of e NOSNO system.
【作者單位】： 重慶醫(yī)科大學藥理學教研室重慶市生物化學與分子藥理學重點實驗室;遵義醫(yī)學院藥理教研室基礎(chǔ)藥理省部共建教育部重點實驗室;重慶科瑞制藥(集團)有限公司;
【基金】：國家自然科學基金資助項目(NO 81100905)
【分類號】：R965

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