| 郭英惠,代红燕,姚雪萍,任 芳,尹 娜,左晓婷.Klotho蛋白对大鼠心肌缺血-再灌注损伤的作用机制探究[J].现代生物医学进展英文版,2024,(19):3616-3618. |
| Klotho蛋白对大鼠心肌缺血-再灌注损伤的作用机制探究 |
| Investigation of the Mechanism of Klotho Protein on Myocardial Ischemia-reperfusion Injury in Rats |
| Received:May 12, 2024 Revised:May 31, 2024 |
| DOI：10.13241/j.cnki.pmb.2024.19.003 |
| 中文关键词: Klotho蛋白 缺血-再灌注损伤 |
| 英文关键词: Klotho protein Ischemia-reperfusion injury |
| 基金项目:新疆维吾尔自治区自然科学基金面上项目（2022D01C446） |
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| 中文摘要: |
| 摘要 目的：探讨Klotho蛋白对大鼠心肌缺血-再灌注损伤的作用机制。方法：选择60只雄性SD大鼠，根据完全随机数字法将60只大鼠分为正常对照组、缺血再灌注损伤+生理盐水组、缺血再灌注损伤+低浓度Klotho蛋白组、缺血再灌注损伤+高浓度Klotho蛋白组，每组15只。分别进行处理，并分析相关血清、蛋白的表达，对比细胞凋亡。结果：血清IL-6、IL-1β、TNF-α、NF-κB、Iκκβ、心脏组织caspase9、ROS、MDA、细胞凋亡：缺血再灌注损伤+生理盐水组>缺血再灌注损伤+低浓度Klotho蛋白组>缺血再灌注损伤+高浓度Klotho蛋白组>正常对照组；血清IκBα、Klotho蛋白、心脏组织Klotho蛋白、caspase3、细胞色素C、Bax/Bcl-2蛋白、三磷酸腺苷、二磷酸腺苷、一磷酸腺苷、SOD：缺血再灌注损伤+生理盐水组<缺血再灌注损伤+低浓度Klotho蛋白组<缺血再灌注损伤+高浓度Klotho蛋白组<正常对照组，P均<0.05。结论：Klotho蛋白可维护心肌线粒体的功能、结构完整，提高心肌组织，减轻炎症反应、氧化应激反应，减少心肌细胞凋亡。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the mechanism of Klotho protein on myocardial ischemia-reperfusion injury in rats. Methods: Sixty male SD rats were selected, and 60 rats were divided into normal control group, ischemia reperfusion injury + saline group, ischemia reperfusion injury + low concentration Klotho protein group, ischemia reperfusion injury + high concentration Klotho protein group, 15 in each group. Treatment was performed separately and the expression of relevant serum and protein was analyzed to contrast apoptosis. Results: The serum IL-6, IL-1β, TNF-α, NF-κB, Iκκβ, caspase9, ROS, MDA, apoptosis: Ischemia-reperfusion injury + normal saline group>ischemia-reperfusion injury + low-concentration Klotho protein group>ischemia-reperfusion injury + high-concentration Klotho protein group>normal control group; Serum IκBα, Klotho protein, Heart tissue Klotho protein, caspase3, Cytochrome C, Bax/Bcl-2 protein, ATP, diphosphate, ATP, SOD: Ischemia-reperfusion injury + normal saline groupConclusion: Klotho protein can maintain the function and structural integrity of myocardial mitochondria, improve myocardial tissue, reduce inflammation and oxidative stress, and reduce cardiomyocyte apoptosis. |
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