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首页> 外文期刊>Journal of Cellular Physiology >Hyperglycemia induces apoptosis via CB1 activation through the decrease of FAAH 1 in retinal pigment epithelial cells.
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Hyperglycemia induces apoptosis via CB1 activation through the decrease of FAAH 1 in retinal pigment epithelial cells.

机译：高血糖通过CB1激活凋亡通过减少FAAH 1视网膜色素上皮细胞。

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摘要

Fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of the main endocannabinoid, anandamide, and related fatty acid amides, has emerged as a regulator of endocannabinoid signaling. Retinal pigment epithelial (RPE) cells are believed to be important cells in the pathogenesis of diabetic retinopathy. However, the pathophysiology of FAAH in diabetic retinopathy has not been determined. Thus, we examined the effect of high glucose (HG) on the expression of FAAH and CB(1)R in the ARPE-19 human RPE cells. We found that HG downregulated the expression of FAAH 1 mRNA and protein in ARPE-19 cells. In contrast, it upregulated the expression of CB(1)R mRNA and protein. HG-induced internalization of CB(1)R in HEK 293 cells and ARPE-19 cells was blocked by overexpression of FAAH 1 and treatment with the CB(1)R blocker, AM 251. HG-induced generation of reactive oxygen species and lipid peroxide formation were blocked by the overexpression of FAAH 1. FAAH 1 overexpression also blocked HG-induced expression of CB(1)R in the cytosolic fraction. We also investigated whether the overexpression of FAAH 1 protected against HG-induced apoptosis. High glucose increased the Bax/Bcl-2 ratio and levels of cleaved PARP, cleaved caspase-9 and caspase-3, and reduced cell viability. HG-induced apoptotic effects were reduced by the overexpression of FAAH 1, treatment with the CB(1)R-specific antagonist AM 251 and CB(1)R siRNA transfection. In conclusion, HG-induced apoptosis in ARPE-19 cells by inducing CB(1)R expression through the downregulation of FAAH 1 expression. Our results provide evidence that CB(1)R blockade through the recovery of FAAH 1 expression may be a potential anti-diabetic therapy for the treatment of diabetic retinopathy.
机译：脂肪酸酰胺水解酶(FAAH)的酶负责主要的降解神经,叫花生四烯酸乙醇胺和脂肪有关酸酰胺,已经成为监管机构神经信号。上皮(RPE)细胞被认为是重要的细胞在糖尿病的发病机制视网膜病变。在糖尿病视网膜病变尚未确定。因此,我们研究了高葡萄糖(HG)的影响在FAAH和CB的表达(1)RARPE-19人类RPE细胞。表达下调FAAH 1 mRNA的表达在ARPE-19细胞蛋白质。调节CB (1) R mRNA的表达蛋白质。HEK 293细胞和ARPE-19细胞被超表达FAAH 1和治疗CB (1) R拦截器,是251年。活性氧和脂质过氧化形成的超表达被封锁FAAH 1。HG-induced CB的表达(1)R在胞质中分数。FAAH 1的过度保护HG-induced细胞凋亡。伯灵顿/ bcl - 2比例和裂解PARP的水平,裂解caspase-9 caspase-3,减少细胞生存能力。减少FAAH 1的过度表达,与CB (1) R-specific拮抗剂治疗251年,小干扰rna转染CB (1) R。HG-induced ARPE-19细胞凋亡诱导CB (1) R的差别通过对这些基因的表达FAAH 1表达。CB (1) R通过恢复FAAH封锁1的表达可能是一个潜在的治疗治疗糖尿病的治疗视网膜病变。

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