ArticleChonnam medical journal2011
Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells.
Article in Chonnam medical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 10 citations in OpenAlex.
- Putative role of natural products as Protein Kinase C modulator in different disease conditions.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2021Review
- Polyphenol compounds and PKC signaling.Biochimica et biophysica acta · 2016Review
- Epigallocatechin-3-gallate attenuates unilateral ureteral obstruction-induced renal interstitial fibrosis in mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2015Article
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5 authors at 1 institution in 1 country.
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Abstract
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.
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