التفاصيل البيبلوغرافية
| العنوان: |
松弛素保护心肌微血管内皮细胞缺氧复氧损伤的机制. |
| Alternate Title: |
Relaxin protects myocardial microvascular endothelial cells from hypoxia-reoxygenation injury. |
| المؤلفون: |
魏 琴1,2, 阿曼古丽·如则2,3, 陈冰心4, 赵 翎2,3, 赵帮豪2,3, 姜 涛2,5, 张 春2,5, 李志强2,5, 高晓明2,3,6, 段明军2,5 |
| المصدر: |
Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu. 10/8/2023, Vol. 27 Issue 28, p4519-4524. 6p. |
| مصطلحات موضوعية: |
*CELL permeability, *CARDIAC hypertrophy, *REPERFUSION injury, *GENE expression, *ENDOTHELIAL cells, *CADHERINS |
| Abstract (English): |
BACKGROUND: Relaxin can significantly improve cardiac and renal dysfuction caused by pathological factors, inhibit myocardial hypertrophy, have an anti-fibrosis effect, and improve ischemia-reperfusion injury. However, its protective mechanism against hypoxia-reoxygenation injury of endothelial cells remains unclear. OBJECTIVE: To investigate the protective mechanism of relaxin against hypoxia-reoxygenation injury of myocardial microvascular endothelial cells. METHODS: Mouse myocardial microvascular endothelial cell line (H5V cells) was used for the experiment. Cells were treated by three different interventions: in control group, cells were normally cultured for 33 hours; in model group, cells were treated by 6-hour hypoxia followed by 3-hour reoxygenation); and in relaxin group, 24 hours of routine culture (180 ng/mL relaxin), 6 hours of hypoxia and 3 hours of reoxygenation (180 ng/mL relaxin) were given to simulate myocardial hypoxia-reperfusion injury. Cell permeability and Caspase-3 activity were then detected. Levels of tumor necrosis factor-α, interleukin-1β and interleukin-6 in cell supernatants were detected by ELISA. Expressions of VE-cadherin, Akt, and GSK-3β at mRNA and protein levels were detected by RT-PCR and western blot, respectively. RESULTS AND CONCLUSION: Compared with the control group, the cell permeability and expression of caspase-3 increased significantly in the model group (P < 0.05). Compared with the model group, the cell permeability and expression of caspase-3 decreased in the relaxin group (P < 0.05). Moreover, the levels of tumor necrosis factor-α, interleukin-1β and interleukin-6 were elevated in the model group, while the levels were significantly decreased after relaxin treatment (all P < 0.05). There were no significantly changes in the mRNA and protein expressions of VE-cadherin, Akt1, and GSK-3β mRNA among three groups (all P > 0.05). Compared with the control group, the expression of phosphorylated VE-cadherin, Akt1 and GSK-3β were decreased in the model group (P < 0.05), and relaxin treatment reversed these changes to the control levels (P < 0.05). To conclude, relaxin treatment could enhance VE-cadherin expression, reduce hypoxiareoxygenation-induced microvascular endothelial cell damage, inhibit inflammatory cytokine release, and reduce cell apoptosis, which may be related to the activation of the Akt/GSK-3β signaling pathway. [ABSTRACT FROM AUTHOR] |
| Abstract (Chinese): |
背景: 研究报道松弛素可显著改善病理因素导致的心肾功能障碍, 抑制心肌肥厚、抗纤维化以及改善缺血再灌注损伤等, 但其对内皮细胞 缺氧复氧损伤的保护机制尚不明确. 目的: 探讨松弛素保护心肌微血管内皮细胞缺氧复氧损伤的机制. 方法: 取生长状态良好的小鼠心肌微血管内皮细胞系(H5V), 分3组处理: 对照组常规培养33 h, 模型组常规培养24 h后给予6 h缺氧+3 h复 氧模拟心肌缺氧再灌注损伤, 松弛素组常规培养(加180 ng/mL松弛素)24 h后给予6 h缺氧+3 h复氧(加180 ng/mL松弛素)模拟心肌缺氧再灌注 损伤. 检测细胞通透性与Caspase-3的表达, 细胞上清中肿瘤坏死因子α、白细胞介素1β和白细胞介素6水平, RT-PCR检测细胞中钙黏蛋白、 Akt1、GSK-3β mRNA表达; Western blot检测细胞中钙黏蛋白、Akt、GSK-3β蛋白表达. 结果与结论: ①与对照组比较, 模型组细胞通透性增强(P < 0.05), 细胞内Caspase-3表达升高(P < 0.05); 与模型组比较, 松弛素组细胞通 透性降低(P < 0.05), 细胞内Caspase-3表达降低(P < 0.05); ②与对照组比较, 模型组上清中肿瘤坏死因子α、白细胞介素1β和白细胞介素 6水平升高(P < 0.05); 与模型组比较, 松弛素组3种炎症因子水平降低(P < 0.05); ③3组间细胞中钙黏蛋白、Akt1、GSK-3β mRNA表达比较 差异无显著性意义(P > 0.05); ④3组间细胞中钙黏蛋白、Akt、GSK-3β总蛋白表达比较差异无显著性意义(P > 0.05); 与对照组比较, 模型 组磷酸化钙黏蛋白、p-Akt、p-GSK-3β蛋白表达降低(P < 0.05); 与模型组比较, 松弛素组磷酸化钙黏蛋白、p-Akt、p-GSK-3β蛋白表达升高 (P < 0.05); ⑤结果表明, 松弛素治疗通过增强钙黏蛋白表达, 减少缺氧复氧引起的小鼠心肌微血管内皮细胞损伤, 抑制炎症因子的释放, 减轻细胞凋亡, 该作用可能与激活Akt/GSK-3β信号通路有关. [ABSTRACT FROM AUTHOR] |
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