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Research Article

亲环蛋白D通过线粒体通透性过渡孔调节急性非结石性胆囊炎的氧化应激和细胞凋亡

卷 23, 期 9, 2023

发表于: 12 October, 2022

页: [971 - 980] 页: 10

弟呕挨: 10.2174/1566524023666220908112922

价格: $65

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摘要

目的:急性非结石性胆囊炎(AAC)具有起病急、进展快、病死率高、并发症多等特点。亲环蛋白D（CypD）调节线粒体通透性转换孔（MPTP），参与缺血再灌注损伤和炎症的发生；然而，CypD 在 AAC 中的作用仍不清楚。 方法:将300~350 g豚鼠随机分为3组,即假手术组、胆总管结扎24h组(CBDL-24h组)、CBDL-48h组。采用Western blot和qRT-PCR分析各组CypD的差异表达，并采用透射电镜检测线粒体结构的变化。通过环孢素A（CsA）抑制CypD的活性，我们利用线粒体肿胀、活性氧（ROS）检测和线粒体膜电位来评估线粒体的差异。 结果：与假手术组相比，CBDL-24h和CBDL-48h组梗阻时间延长，胆囊炎症加重，CypD表达上调。 CBDL-24h和48h组线粒体肿胀程度增加，MPTP开放时间延长。减少 CypD 的表达可以抑制 MPTP 的开放，防止线粒体膜电位的操纵，并最终降低细胞内 ROS 和细胞凋亡的水平。 结论：CypD通过调节MPTP的开放在AAC的发生发展中发挥促炎作用。抑制CypD的活性可以降低ROS水平和细胞凋亡，挽救线粒体功能，最终缓解AAC。因此，CypD可能作为ACC的潜在治疗靶点。

关键词: 亲环蛋白D，线粒体通透性过渡孔，环孢菌素A，急性非结石性胆囊炎，氧化应激，细胞凋亡。

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