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章林明.G 蛋白偶联雌激素受体可通过抑制氧化应激反应减轻肾缺血再灌注损伤[J].中国比较医学杂志,2020,30(6):10~16,24.
G 蛋白偶联雌激素受体可通过抑制氧化应激反应减轻肾缺血再灌注损伤
G protein-coupled estrogen receptor alleviates renal ischemia reperfusion injury by inhibiting oxidative stress
投稿时间:2019-11-28  
DOI:10. 3969 / j.issn.1671-7856. 2020. 06. 002
中文关键词:  G 蛋白偶联雌激素受体  缺血再灌注损伤  氧化应激反应  超氧化物歧化酶
英文关键词:G protein-coupled estrogen receptor  ischemia reperfusion  oxidative stress  superoxide dismutase
基金项目:
作者单位E-mail
章林明 石河子大学医学院,新疆 石河子 832000 897865531@ qq.com 
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中文摘要:
      目的 探讨 G 蛋白偶联雌激素受体(G protein-coupled estrogen receptor, GPER)对氧化应激反应的影响,及其对肾缺血再灌注损伤的保护作用和可能机制。 方法 将雌性 SD 大鼠去卵巢后随机分为去卵巢组 (OVX)、肾缺血再灌注组(OVX+I/ R)、雌激素干预组(OVX+I/ R+E2 )、GPER 特异性激动剂 G1 干预组(OVX+I/ R+ G1)、雌激素+GPER 特异性阻断剂 G15 干预组(OVX+I/ R+G15+E2 ) (每组 8 只)。测定各组大鼠血肌酐(Cr)和尿素氮(BUN)水平,HE 染色观察肾组织病理性形态,检测各组肾组织中超氧化物歧化酶( SOD) 活性及丙二醛 (MDA)含量,Western blot 检测肾组织 p-PI3K、p-Akt 蛋白的表达水平。 结果 与 OVX 组相比,OVX+I/ R 组血 Cr 和 BUN 水平升高(P< 0. 01),肾组织病理损伤(HE 染色)明显(P< 0. 01),氧化应激反应加重(P< 0. 01),p-PI3K、p-Akt 蛋白表达水平显著降低(P< 0. 01);与 OVX+I/ R 组相比,E2 和 G1 干预组血 Cr 和 BUN 水平降低(P< 0. 01),肾组织病理损伤减轻(P< 0. 01),氧化应激反应减轻(P< 0. 01),p-PI3K、p-Akt 蛋白表达水平升高(P< 0. 01),而 GPER 特异性阻断剂 G15 可部分消除 E2 对肾缺血再灌注损伤的保护作用。 结论 E2 和 GPER 激动剂 G1 可降低氧化应激反 应,减轻大鼠肾缺血再灌注损伤,且 E2 对 I/ R 的保护作用可能通过 GPER 介导,其机制可能涉及 PI3K/ Akt 信号通路的激活。
英文摘要:
      Objective To investigate the effect of the G protein-coupled estrogen receptor (GPER) on oxidative stress and its possible mechanisms for reducing renal ischemia reperfusion injury. Methods Female ovariectomized rats were divided into the ovariectomy (OVX), renal ischemia reperfusion (OVX+I/ R), estrogen intervention (OVX+I/ R+E2 ), GPER-specific agonist (G1) intervention (OVX+I/ R+G1), and estrogen+GPER specific blocker G15 intervention (OVX+I/ R+G15+ E2 ) groups ( n= 8 rats per group). Serum creatinine ( Cr) and urea nitrogen ( BUN) levels were measured, and histopathological examination using hematoxylin and eosin ( HE) staining was used to observe the pathological morphology of the renal tissues. Superoxide dismutase and malondialdehyde activities were detected, and Western blot was used to observe p-PI3K and p-Akt expressions in the renal tissues of each group. Results Compared with the OVX group, serum Cr and BUN levels were increased, pathological damage to the renal tissue was significant, oxidative stress was aggravated, and p-PI3K and p-Akt protein expression levels were significantly decreased in the OVX+I/ R group (allP< 0. 01). Compared with the OVX + I/ R group, the serum Cr and BUN levels were decreased, renal tissue pathological damage was reduced, oxidative stress was reduced, p-PI3K and p-Akt protein expressions were increased (all P< 0. 01), and the GPER-specific inhibitor, G15, partially eliminated the protective effect of E2 on renal ischemia reperfusion injury in the E2 and G1 intervention groups. Conclusions During renal ischemia reperfusion injury, E2 and G1 may reduce oxidative stress to alleviate the injury. GPER may mediate the protective effect of E2 , and its mechanism may involve activating the PI3K/ Akt signaling pathway.
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