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转化生长因子-β可阻断葡萄糖诱导的角膜上皮细胞炎症和凋亡。

Transforming growth factor-β blocks glucose-induced inflammation and apoptosis in corneal epithelial cells.

作者信息

Liu Fengge, Kong Hui, Kong Xiangfeng

机构信息

Department of Ophthalmology Zoucheng People's Hospital China.

出版信息

FEBS Open Bio. 2018 Nov 6;8(12):1936-1942. doi: 10.1002/2211-5463.12529. eCollection 2018 Dec.

DOI:10.1002/2211-5463.12529
PMID:30524944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6275247/
Abstract

Diabetic retinopathy is the most important ocular complication associated with diabetes. Corneal defects due to diabetes mellitus (DM) may cause severe vision impairments. This study aimed to identify the effect of transforming growth factor-β (TGF-β) on biological events, such as apoptosis and inflammation, in the diabetic cornea. High-glucose treatment induced reactive oxygen species (ROS) production and several biological events, including apoptosis and inflammatory cytokine secretion, in human corneal epithelial cells. However, administration of TGF-β significantly decreased ROS production, Annexin V-positive cells, and levels of inflammatory cytokines. Sprague Dawley rats were injected with streptozotocin (STZ) as a model of DM. Inflammatory cytokine secretion, apoptosis, and inflammation were all increased by STZ treatment. However, apoptosis and inflammation were markedly reduced following TGF-β treatment. In conclusion, TGF-β can ameliorate the enhancement of apoptosis and inflammation in diabetic cornea in and .

摘要

糖尿病性视网膜病变是与糖尿病相关的最重要的眼部并发症。糖尿病（DM）导致的角膜缺陷可能会引起严重的视力损害。本研究旨在确定转化生长因子-β（TGF-β）对糖尿病角膜中细胞凋亡和炎症等生物学事件的影响。高糖处理可诱导人角膜上皮细胞产生活性氧（ROS）以及多种生物学事件，包括细胞凋亡和炎性细胞因子分泌。然而，给予TGF-β可显著降低ROS产生、膜联蛋白V阳性细胞以及炎性细胞因子水平。将链脲佐菌素（STZ）注射到斯普拉格-道利大鼠体内作为糖尿病模型。STZ处理可使炎性细胞因子分泌、细胞凋亡和炎症均增加。然而，TGF-β处理后细胞凋亡和炎症明显减轻。总之，TGF-β可改善体内和体外糖尿病角膜中细胞凋亡和炎症的增强情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/133584c2fa19/FEB4-8-1936-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/51584ac43caa/FEB4-8-1936-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/e775dd62c588/FEB4-8-1936-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/52c37364fc12/FEB4-8-1936-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/133584c2fa19/FEB4-8-1936-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/51584ac43caa/FEB4-8-1936-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/58f08ac4cd55/FEB4-8-1936-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/a89ff82fe166/FEB4-8-1936-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/e775dd62c588/FEB4-8-1936-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/52c37364fc12/FEB4-8-1936-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d1/6275247/133584c2fa19/FEB4-8-1936-g006.jpg

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