| 巩 亮,王晓春,焦 阳,姜顺涛,杨光磊.达格列净对高血压小鼠小动脉重构的影响及机制[J].现代生物医学进展英文版,2022,(8):1429-1433. |
| 达格列净对高血压小鼠小动脉重构的影响及机制 |
| The Effect and Mechanism of Dapagliflozin on Arteriole Remodeling in Hypertensive Mice |
| Received:October 07, 2021 Revised:October 31, 2021 |
| DOI：10.13241/j.cnki.pmb.2022.08.006 |
| 中文关键词: 达格列净 高血压 小动脉重构 PI3K / Akt 信号通路 |
| 英文关键词: Dapagliflozin Hypertension Arteriole remodeling PI3K/Akt Signaling pathway |
| 基金项目:贵州省科技厅基金项目（黔科合基础[2016]1173） |
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| 中文摘要: |
| 摘要 目的：探究钠葡萄糖共转运蛋白2抑制剂（达格列净）对高血压小鼠小动脉重构的影响及机制。方法：30只12周龄的C57BL / 6雄性小鼠纳入本研究，根据实验目的将实验小鼠分为对照组、模型组和达格列净组。检测并比较各组小鼠心脏肥大、心脏纤维化、动脉重塑、炎症因子mRNA表达、PI3K和Akt蛋白质表达以及细胞活力和细胞迁移。结果：与对照组相比，模型组收缩压和心脏/体重增加（P<0.05）。与模型组相比，达格列净组收缩压和心脏/体重降低（P<0.05）。与对照组相比，模型组RV/（LV+S）和得分增加（P<0.05）。与模型组相比，达格列净组RV/（LV+S）和得分降低（P<0.05）。与对照组相比，模型组显示血管壁增厚，透明质改变，脑小动脉管腔狭窄或闭塞（P<0.05）。与模型组相比，达格列净组降低高血压引起的小动脉重塑（P<0.05）。与对照组相比，模型组IL-1β，IL-6和TNF-α的mRNA表达水平增加（P<0.05）。与模型组相比，达格列净组IL-1β，IL-6和TNF-α的mRNA表达水平降低（P<0.05）。与对照组相比，模型组PI3K和Akt蛋白质表达水平增加（P<0.05）。与模型组相比，达格列净组PI3K和Akt蛋白质表达水平降低（P<0.05）。与对照组相比，模型组VEZF1，Angpt-1和IGF1表达水平降低（P<0.05）。与模型组相比，达格列净组VEZF1，Angpt-1和IGF1表达水平增加（P<0.05）。与对照组相比，模型组细胞活力和细胞迁移降低（P<0.05）。与模型组相比，达格列净组细胞活力和细胞迁移增加（P<0.05）。结论：达格列净通过抑制PI3K / Akt信号通路，降低炎症反应，增加血管生成能力，降低高血压小鼠小动脉重构。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect and mechanism of sodium-glucose cotransporter 2 inhibitor (dapagliflozin) on arteriole remodeling in hypertensive mice. Methods: Thirty 12-week-old C57BL/6 male mice were included in this study. According to the purpose of the experiment, the experimental mice were divided into control group, model group and dapagliflozin group. Cardiac hypertrophy, cardiac fibrosis, arterial remodeling, inflammatory factor mRNA expression, PI3K and Akt protein expression, cell viability and cell migration were detected and compared in each group of mice. Results: Compared with the control group, the systolic blood pressure and heart/weight increase in the model group(P<0.05). Compared with the model group, the systolic blood pressure and heart/body weight of the dapagliflozin group decreased(P<0.05). Compared with the control group, the model group's RV/(LV+S) and score increased(P<0.05). Compared with the model group, the RV/(LV+S) and score of dapagliflozin group decreased (P<0.05). Compared with the control group, the model group showed thickening of the vessel wall, changes in hyaline, and stenosis or occlusion of cerebral arterioles(P<0.05). Compared with the model group, the dapagliflozin group reduced arterial remodeling caused by hypertension (P<0.05). Compared with the control group, the mRNA expression levels of IL-1β, IL-6 and TNF-α in the model group increased(P<0.05). Compared with the model group, the mRNA expression levels of IL-1β, IL-6 and TNF-α in the dapagliflozin group were reduced (P<0.05). Compared with the control group, the protein expression levels of PI3K and Akt in the model group increased(P<0.05). Compared with the model group, the protein expression levels of PI3K and Akt in the dapagliflozin group decreased (P<0.05). Compared with the control group, the expression levels of VEZF1, Angpt-1 and IGF1 in the model group were reduced(P<0.05). Compared with the model group, the expression levels of VEZF1, Angpt-1 and IGF1 in the dapagliflozin group increased(P<0.05). Compared with the control group, the cell viability and cell migration of the model group were reduced(P<0.05). Compared with the model group, the cell viability and cell migration of the dapagliflozin group increased (P<0.05). Conclusion: Dapagliflozin inhibits PI3K/Akt signaling pathway, reduces inflammation, increases angiogenesis, and reduces arteriolar remodeling in hypertensive mice. |
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