郝艳.司美格鲁肽改善糖尿病患者心肌纤维化[J].内科急危重症杂志,2025,31(4):311-315
|
DOI:10.11768/nkjwzzzz20250404 |
中文关键词: 司美格鲁肽 2型糖尿病 心肌纤维化 心脏磁共振 |
英文关键词: |
基金项目:无锡市科技发展基金项目(K20221041) |
|
摘要点击次数: 10 |
全文下载次数: 15 |
中文摘要: |
摘要 目的:应用心脏磁共振(CMR)评价司美格鲁肽改善2型糖尿病(T2DM)患者心肌纤维化的疗效及对肌醇3-激酶(PI3K)/蛋白激酶B(Akt)/内皮型一氧化氮(eNOS)通路的影响。方法:前瞻性选择T2DM合并心肌纤维化患者52例,采用随机数字表法分为对照组和观察组各26例。对照组采用二甲双胍和胰岛素治疗,观察组在对照组基础上予以司美格鲁肽,连续治疗12个月。应用CMR扫描检测左心室射血分数(LVEF)、舒张末期容积指数(LVEDVI)、左心室质量指数(LVMMI)、心肌细胞外容积分数(ECV)和T1值;酶联免疫吸附法检测血清半乳糖凝集素-3(Gal-3)和基质金属蛋白酶-2(MMP-2);蛋白印迹法检测血清p-PI3K、p-Akt和p-eNOS蛋白相对表达量;以及血糖控制情况。结果:治疗前2组各项指标无显著差异(P均>0.05);治疗后观察组LVEDVI、LVMMI、血清Gal-3和MMP-2水平、ECV和T1值以及血清p-PI3K、p-Akt和p-eNOS蛋白相对表达量下降,LVEF升高(P均<0.05),对照组改善不明显(P>0.05)。治疗后2组空腹血糖、餐后2h血糖、糖化血红蛋白及体质量指数均下降,且观察组较对照组显著降低(P均<0.05)。2组不良反应事件发生率比较,无统计学差异(P>0.05)。结论:司美格鲁肽治疗T2DM患者能明显改善心肌纤维化程度和心功能,且不增加低血糖风险,其机制可能与PI3K/Akt/eNOS信号通路活性被抑制有关。 |
英文摘要: |
Abstract Objective: To evaluate the clinical efficacy of semaglutide in the treatment of type 2 diabetes mellitus (T2DM) patients with myocardial fibrosis by cardiac magnetic resonance (CMR) and effects on phosphoinositide 3-kinase (PI3K)/Akt/eNOS pathway. Methods A total of 52 cases of T2DM with myocardial fibrosis diagnosed in our hospital by the method of digital random table were selected as the study subjects. They were randomly divided into control group and observation group, with 26 patients in each group. The control group received metformin and insulin, while the observation group received semaglutide for 12 months on the basis of control group. The LVEF, end-diastolic volume index (LVEDVI), and left ventricular mass index (LVMI) were obtained using CMR black blood, bright blood, and late gadolinium enhancement (LGE) sequences, as well as ECV and T1 score. The serum myocardial fibrosis indicators [Galactin-3 (Gal-3) and matrix metalloproteinase-2 (MMP-2)] were measured using ELISA, the relative expression levels of p-PI3K, p-Akt, and p-eNOS proteins were measured using Western blotting, and blood sugar control and body control were compared. Results: All indexes between two groups showed no significant difference before therapy (P>0.05). The indexes of LVEDVI, LVMI, and serum levels of Gal-3 and MMP-2, ECV and T1 score in the observation group after therapy were lower than those before therapy (P<0.05), while LVEF was increased (P<0.05). After treatment, fasting blood glucose, 2-h postprandial blood glucose, glycated hemoglobin and BMI in both groups decreased compared to pre-treatment, and those in the observation group significantly decreased compared to the control group (P< 0.05). The occurrences of adverse reaction events had no significant difference between two groups (P> 0.05). Conclusion: Semaglutide in the treatment of T2DM with myocardial fibrosis can significantly improve the degree of myocardial fibrosis and cardiac function, which may be related to the inhibition of PI3K/Akt/eNOS signal pathway activity, does not increase the risk of hypoglycemia, and its application is safe. |
|
|
|
|