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亚甲蓝通过激活 Sirtuin 1 减少糖尿病视网膜病变大鼠模型中的视网膜细胞炎症、细胞凋亡和氧化应激。

Methylene Blue Reduces Retinal Cell Inflammation, Apoptosis, and Oxidative Stress in a Rat Model of Diabetic Retinopathy via Sirtuin 1 Activation.

出版信息

Altern Ther Health Med. 2023 Nov;29(8):156-165.

Abstract

OBJECTIVE

Diabetic retinopathy (DR), characterized by neuronal damage in the retina, is primarily driven by oxidative stress resulting from diabetes (DM). This study investigated the potential effects of methylene blue (MB) on streptozotocin (STZ)-induced DR.

METHODS

A rat model of DR was established via STZ injection, while a cell model was created using high-glucose (HG) exposure of human retinal microvascular endothelial cells. Evaluation of oxidative stress markers, pro-inflammatory cytokines, and pro-apoptotic proteins was performed based on their expression profiles in human retinal microvascular endothelial cells.

RESULTS

MB treatment significantly upregulated the expression of sirtuin 1 (SIRT1), which was found to be downregulated in the retinal tissues of STZ-treated rats and HG-exposed human retinal microvascular endothelial cells, as determined by polymerase chain reaction (PCR). Furthermore, MB therapy effectively suppressed STZ-induced oxidative stress, inflammation, and cell death. Consistent with the in vivo findings, MB activated the expression of SIRT1, thereby protecting HG-treated human retinal microvascular endothelial cells against oxidative stress, inflammation, and apoptosis.

CONCLUSION

These results support the conclusion that MB mitigates DR by activating SIRT1, leading to a reduction of inflammation, apoptosis, and oxidative stress.

摘要

目的

糖尿病视网膜病变(DR)的特征是视网膜神经元损伤,主要由糖尿病(DM)引起的氧化应激驱动。本研究探讨了亚甲蓝(MB)对链脲佐菌素(STZ)诱导的 DR 的潜在影响。

方法

通过 STZ 注射建立 DR 大鼠模型,通过高糖(HG)暴露于人视网膜微血管内皮细胞建立细胞模型。根据人视网膜微血管内皮细胞的表达谱,评估氧化应激标志物、促炎细胞因子和促凋亡蛋白的表达。

结果

MB 处理显著上调了沉默调节蛋白 1(SIRT1)的表达,聚合酶链反应(PCR)显示 SIRT1 在 STZ 处理大鼠的视网膜组织和 HG 暴露的人视网膜微血管内皮细胞中表达下调。此外,MB 治疗有效抑制了 STZ 诱导的氧化应激、炎症和细胞死亡。与体内研究结果一致,MB 激活了 SIRT1 的表达,从而保护 HG 处理的人视网膜微血管内皮细胞免受氧化应激、炎症和细胞凋亡的影响。

结论

这些结果支持 MB 通过激活 SIRT1 减轻 DR 的结论,从而减少炎症、细胞凋亡和氧化应激。

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