Ginsenoside Rg-1 protects retinal pigment epithelium (RPE) cells from cobalt chloride (CoCl2) and hypoxia assaults.
Ginsenoside Rg-1 protects retinal pigment epithelium (RPE) cells from cobalt chloride (CoCl2) and hypoxia assaults.
复制标题
人参皂苷 Rg-1 保护视网膜色素上皮 (RPE) 细胞免受氯化钴 (CoCl2) 和缺氧攻击
DOI：
10.1371/journal.pone.0084171
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Jiang Q
中科院分区：
文献类型：
--
作者：
Li KR;Zhang ZQ;Yao J;Zhao YX;Duan J;Cao C;Jiang Q
严重的视网膜缺血会导致眼部疾病导致持续的视力障碍。视网膜色素上皮（RPE）细胞位于脉络膜毛细血管附近，很容易受到缺血或缺氧的影响。人参皂苷 Rg-1 显示出显着的神经保护作用。本研究旨在测试人参皂苷 Rg-1 在 RPE 细胞中对抗缺氧和氯化钴 (CoCl2) 攻击的细胞保护作用，并了解其潜在机制。我们发现Rg-1预给药显着抑制CoCl2和缺氧诱导的RPE细胞死亡和凋亡。 CoCl2 诱导的 RPE 细胞死亡需要活性氧特异性 (ROS) 依赖性 p38 和 c-Jun NH(2) 末端激酶 (JNK) MAPK 激活，Rg-1 预处理显着抑制 ROS 产生和 p38/JNK 激活。此外，CoCl2 通过激活 AMP 激活蛋白激酶 (AMPK) 抑制 RPE 细胞中促生存 mTOR 复合物 1 (mTORC1) 的激活，而 Rg-1 通过抑制 AMPK 激活来恢复 mTORC1 活性。 CoCl2 诱导的 AMPK 激活还依赖于 ROS 的产生，抗氧化剂 N-乙酰半胱氨酸 (NAC) 可以防止 CoCl2 引起的 AMPK 激活和 RPE 细胞死亡。我们的结果表明，Rg-1 可以作为一种新型的视网膜缺血细胞保护剂进行进一步研究。
Severe retinal ischemia causes persistent visual impairments in eye diseases. Retinal pigment epithelium (RPE) cells are located near the choroidal capillaries, and are easily affected by ischemic or hypoxia. Ginsenoside Rg-1 has shown significant neuroprotective effects. This study was performed to test the cytoprotective effect of ginsenoside Rg-1 in RPE cells against hypoxia and cobalt chloride (CoCl2) assaults, and to understand the underlying mechanisms. We found that Rg-1 pre-administration significantly inhibited CoCl2- and hypoxia-induced RPE cell death and apoptosis. Reactive oxygen specisis (ROS)-dependent p38 and c-Jun NH(2)-terminal kinases (JNK) MAPK activation was required for CoCl2-induced RPE cell death, and Rg-1 pre-treatment significantly inhibited ROS production and following p38/JNK activation. Further, CoCl2 suppressed pro-survival mTOR complex 1 (mTORC1) activation in RPE cells through activating of AMP-activated protein kinase (AMPK), while Rg-1 restored mTORC1 activity through inhibiting AMPK activation. CoCl2-induced AMPK activation was also dependent on ROS production, and anti-oxidant N-acetylcysteine (NAC) prevented AMPK activation and RPE cell death by CoCl2. Our results indicated that Rg-1 could be further investigated as a novel cell-protective agent for retinal ischemia.
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活化的蛋白 C 可将视网膜从缺血引起的细胞死亡中拯救出来。
影响因子：
4.4
作者：
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