Methionine restrictive diet may alleviate ischaemia/reperfusion (I/R)‐induced myocardial injury, but its underlying mechanism remains unclear. HE staining was performed to evaluate the myocardial injury caused by I/R and the effect of methionine‐restricted diet (MRD) in I/R mice. IHC and Western blot were carried out to analyse the expression of CSE, CHOP and active caspase3 in I/R mice and hypoxia/reoxygenation (H/R) cells. TUNEL assay and flow cytometry were used to assess the apoptotic status of I/R mice and H/R cells. MTT was performed to analyse the proliferation of H/R cells. H2S assay was used to evaluate the concentration of H2S in the myocardial tissues and peripheral blood of I/R mice. I/R‐induced mediated myocardial injury and apoptosis were partially reversed by methionine‐restricted diet (MRD) via the down‐regulation of CSE expression and up‐regulation of CHOP and active caspase3 expression. The decreased H2S concentration in myocardial tissues and peripheral blood of I/R mice was increased by MRD. Accordingly, in a cellular model of I/R injury established with H9C2 cells, cell proliferation was inhibited, cell apoptosis was increased, and the expressions of CSE, CHOP and active caspase3 were dysregulated, whereas NaHS treatment alleviated the effect of I/R injury in H9C2 cells in a dose‐dependent manner. This study provided a deep insight into the mechanism underlying the role of MRD in I/R‐induced myocardial injury.

中文翻译：

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膳食蛋氨酸限制通过激活糖尿病小鼠的 CSE/H2S/ERS 通路来减轻肾缺血/再灌注诱导的心肌损伤。

蛋氨酸限制性饮食可以减轻缺血/再灌注（I/R）诱导的心肌损伤，但其潜在机制尚不清楚。进行HE染色以评估I / R引起的心肌损伤和I / R小鼠中蛋氨酸限制饮食（MRD）的影响。进行IHC和Western印迹分析CSE、CHOP和活性caspase3在I/R小鼠和缺氧/复氧(H/R)细胞中的表达。TUNEL 测定和流式细胞术用于评估 I/R 小鼠和 H/R 细胞的凋亡状态。进行MTT以分析H/R细胞的增殖。H2S测定用于评估I/R小鼠心肌组织和外周血中H2S的浓度。甲硫氨酸限制饮食（MRD）通过下调 CSE 表达和上调 CHOP 和活性 caspase3 表达，部分逆转 I/R 介导的心肌损伤和细胞凋亡。MRD增加了I/R小鼠心肌组织和外周血中H2S浓度的降低。因此，在用H9C2细胞建立的I/R损伤细胞模型中，细胞增殖受到抑制，细胞凋亡增加，CSE、CHOP和活性caspase3的表达失调，而NaHS处理减轻了I/R损伤的影响。在 H9C2 细胞中呈剂量依赖性。该研究深入了解了 MRD 在 I/R 诱导的心肌损伤中的作用机制。MRD增加了I/R小鼠心肌组织和外周血中H2S浓度的降低。因此，在用H9C2细胞建立的I/R损伤细胞模型中，细胞增殖受到抑制，细胞凋亡增加，CSE、CHOP和活性caspase3的表达失调，而NaHS处理减轻了I/R损伤的影响。在 H9C2 细胞中呈剂量依赖性。该研究深入了解了 MRD 在 I/R 诱导的心肌损伤中的作用机制。MRD增加了I/R小鼠心肌组织和外周血中H2S浓度的降低。因此，在用H9C2细胞建立的I/R损伤细胞模型中，细胞增殖受到抑制，细胞凋亡增加，CSE、CHOP和活性caspase3的表达失调，而NaHS处理减轻了I/R损伤的影响。在 H9C2 细胞中呈剂量依赖性。该研究深入了解了 MRD 在 I/R 诱导的心肌损伤中的作用机制。而 NaHS 治疗以剂量依赖性方式减轻了 H9C2 细胞中 I/R 损伤的影响。该研究深入了解了 MRD 在 I/R 诱导的心肌损伤中的作用机制。而 NaHS 治疗以剂量依赖性方式减轻了 H9C2 细胞中 I/R 损伤的影响。该研究深入了解了 MRD 在 I/R 诱导的心肌损伤中的作用机制。