| 4-甲酚减轻糖尿病大鼠心肌缺血/再灌注损伤 |
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| 引用本文： | 刘力华,王东,张美艳,吴杨鹏,邢甜甜,王小闯.4-甲酚减轻糖尿病大鼠心肌缺血/再灌注损伤[J].心脏杂志,2023,35(1):9-14. |
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| 作者姓名： | 刘力华 王东 张美艳 吴杨鹏 邢甜甜 王小闯 |
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| 作者单位： | 1.急诊科 西安市第三医院 |
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| 摘 要： | 目的 旨在研究4-甲酚对糖尿病(diabetic mellitus, DM)大鼠心肌缺血/再灌注（myocardial ischemiareperfusion, MI/R）损伤的保护作用，并初步探讨其机制。方法 取雄性SD大鼠，分为正常对照组和糖尿病组。利用高脂饲料联合链脲霉素诱导2型糖尿病大鼠模型。造模成功后，随即分为3组：糖尿病假手术组（DM+Sham）、糖尿病心肌缺血/再灌注组（DM+MI/R）和糖尿病心肌缺血/再灌注+4-甲酚组（DM+MI/R+4-cresol）。4-cresol组采用植入式胶囊渗透压泵给药（5.5 mmol/L 4-cresol,0.15μL/h），其余给予生理盐水。6周后，采用结扎冠状动脉左前降支30 min再灌注3 h的方法建立心肌缺血/再灌注模型。再灌注结束处死大鼠，检测心肌梗死和细胞凋亡。检测心肌氧化应激程度。测定心肌双底物特异性酪氨酸磷酸化调节激酶1a(dual specificity tyrosinephosphorylation-regulated kinase 1A, Dyrk1A)表达以及细胞凋亡信号调节激酶1(apoptosis sign...
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| 关 键 词： | 4-甲酚 细胞凋亡 氧化应激 糖尿病心肌 心肌缺血/再灌注 |
| 收稿时间： | 2022-03-22 |
Gut microbial metabolite 4-cresol attenuates myocardial ischemia/reperfusion injury in diabetes |
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| Affiliation: | 1.Department of Emergency2.Department of Cardiology3.Department of Pediatrics, Xi’an Third Hospital, Xi’an 710018, Shaanxi, China4.Department of Critical Care Medicine, Second Affiliated Hospital, Xi’an Jiaotong University, Xi’an 710004, Shaanxi, China |
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| Abstract: | AIM To observe the protective effect of 4-cresol on diabetic hearts following ischemia/reperfusion (I/R) and to explore the possible molecular mechanisms. METHODS Forty-six male SD rats were randomly divided into normal control (CON) group and diabetes mellitus (DM) group. The DM rat model was induced by high-fat diet combined with a low-dose intraperitoneal injection of streptozotocin. Diabetic rats were randomly subdivided into three groups: Sham-operated DM rats (DM+Sham), DM+MI/R, and DM+MI/R+4-cresol (5.5 mmol/L 4-cresol, 0.15 μL/h). The MI/R model was established by coronary artery ligation. After 30 min of ischemia, the myocardium was reperfused for 3 h. RESULTS 4-cresol significantly attenuated myocardial injury in diabetes as evidenced by decreased infarct size, serum CK and LDH activities and cell apoptosis. Moreover, 4-cresol increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased malonaldehyde (MDA) in I/R hearts (P<0.05, P<0.01). Additionally, 4-cresol supplementation markedly inhibited dual specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A) expression and decreased the phosphorylation of apoptosis signal-regulating kinase 1 (ASK1) (P<0.05, P<0.01). CONCLUSION 4-cresol effectively inhibits Dyrk1A expression, reduces oxidative stress and cardiomyocyte apoptosis and eventually alleviates MI/R injury in diabetic hearts. |
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