首页> 美国卫生研究院文献>Chonnam Medical Journal >Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1 PKC α/βII and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells
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Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1 PKC α/βII and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells

机译:表没食子儿茶素-3-没食子酸酯对高糖刺激的肾小球上皮细胞中TGF-β1PKCα/βII和NF-κB表达的影响

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摘要

Epigallocatechin-3-gallate (EGCG) is the most potent antioxidant polyphenol in green tea. In the present study, we investigated whether EGCG plays a role in the expression of transforming growth factor-beta1 (TGF-β1), protein kinase C (PKC) α/βII, and nuclear factor-kappaB (NF-κB) in glomerular epithelial cells (GECs) against high-glucose injury. Treatment with high glucose (30 mM) increased reactive oxygen species (ROS)/lipid peroxidation (LPO) and decreased glutathione (GSH) in GECs. Pretreatment with 100 µM EGCG attenuated the increase in ROS/LPO and restored the levels of GSH, whereas ROS, LPO, and GSH levels were not affected by treatment with 30 mM mannitol as an osmotic control. Interestingly, high-glucose treatment affected 3 separate signal transduction pathways in GECs. It increased the expression of TGF-β1, PKC α/βII, and NF-κB in GECs, respectively. EGCG (1, 10, 100 µM) pretreatment significantly decreased the expression of TGF-β1 induced by high glucose in a dose-dependent manner. In addition, EGCG (100 µM) inhibited the phosphorylation of PKC α/βII caused by glucose at 30 mM. Moreover, EGCG (1, 10, 100 µM) pretreatment significantly decreased the transcriptional activity of NF-κB induced by high glucose in a dose-dependent manner. These data suggest that EGCG could be a useful factor in modulating the injury to GECs caused by high glucose.
机译:Epigallocatechin-3-gallate(EGCG)是绿茶中最有效的抗氧化剂多酚。在本研究中,我们调查了EGCG是否在肾小球上皮细胞中的转化生长因子-β1(TGF-β1),蛋白激酶C(PKC)α/βII和核因子-κB(NF-κB)的表达中起作用细胞(GECs)抵抗高糖损伤。用高葡萄糖(30 mM)处理可提高GEC中的活性氧(ROS)/脂质过氧化(LPO)和降低谷胱甘肽(GSH)。用100 µM EGCG预处理可减弱ROS / LPO的增加并恢复GSH的水平,而ROS,LPO和GSH的水平不受30 mM甘露醇作为渗透控制剂的影响。有趣的是,高糖治疗影响了GEC中的3条独立的信号转导途径。它分别增加了GECs中TGF-β1,PKCα/βII和NF-κB的表达。 EGCG(1、10、100 µM)预处理以剂量依赖性方式显着降低高葡萄糖诱导的TGF-β1的表达。此外,EGCG(100 µM)抑制了30 mM葡萄糖引起的PKCα/βII的磷酸化。此外,EGCG(1、10、100 µM)预处理以剂量依赖的方式显着降低了高糖诱导的NF-κB的转录活性。这些数据表明,EGCG可能是调节高糖引起的GEC损伤的有用因素。

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