Impact of EGCG Supplementation on the Progression of Diabetic Nephropathy in Rats: An Insight into Fibrosis and Apoptosis

Abstract

Apoptosis is an active response of cells to altered microenvironments, which is characterized by cell shrinkage, chromatin condensation, and DNA fragmentation, in a variety of cell types such as renal epithelial cells, endothelial cells, mesangial cells, and podocytes. Hyperglycemia is among the microenvironmental factors that may facilitate apoptosis, which plays a decisive role in the initiation of diabetic nephropathy. Transforming growth factor-β emerges as a powerful fibrogenic factor in the development of renal hypertrophy. Although, a number of potential treatment strategies exist for diabetic nephropathy, considering the ease of use and bioavailability, phytochemicals stands distinct as the preeminent option. EGCG, a green tea catechin is one such phytochemical which possesses hypoglycemic and antifibrotic activity. The present study aims to explore the potential of EGCG to prevent apoptosis in a high-fat diet and STZ induced diabetic nephropathy rats by assessing renal function, pro-fibrotic marker, and the expression of apoptotic and antiapoptotic proteins. Our results validate EGCG as a potential antiapoptotic agent evidently by improving renal function via down regulating TGF-β, consequently ameliorating diabetic nephropathy. In accordance with this, EGCG might be regarded as a prospective therapeutic candidate in modulating diabetic nephropathy, thus being a promising treatment.

Candesartan and epigallocatechin‐3‐gallate ameliorate gentamicin‐induced renal damage in rats through p38‐MAPK and NF‐κB pathways

“…This result is in line with Samarghandian et al These cytokines were significantly reduced in candesartan or EGCG‐treated groups. These outcomes are in accordance with others which reported the impact of candesartan on proinflammatory markers; also others reported the anti‐inflammatory effects of EGCG …”

“…also others reported the anti-inflammatory effects of EGCG. [21,48] For additional molecular elucidation of the anti-inflammatory and antiapoptotic responses induced by candesartan and/or EGCG, the kidney content of NF-κB p65 and p38-MAPK, as well as caspase-3, were evaluated. Numerous signaling pathways are involved in controlling apoptosis.…”

“…It is accounted to be responsible for the significant medical benefits of green tea. EGCG has antioxidant, antiapoptotic and anti‐inflammatory features, that are displayed by the direct or indirect involvement of numerous molecules and transduction pathways in cells . Previous studies suggested that EGCG inhibited NF‐κB activation and reduced the activity of p38‐MAPK to prevent various diseases .…”

“…EGCG has antioxidant, antiapoptotic and anti-inflammatory features, that are displayed by the direct or indirect involvement of numerous molecules and transduction pathways in cells. [18][19][20][21] Previous studies suggested that EGCG inhibited NF-κB activation and reduced the activity of p38-MAPK to prevent various diseases. [22,23] To the best of our background, there was no past work that investigated the impact of candesartan and /or EGCG in gentamicin-induced nephrotoxicity.…”

Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice

“…This includes prevention of oxidative injury in cultured endothelial cell lines via the downregulation of intercellular adhesion molecule 1 expression and 4-hydroxynonenal accumulation, and restoration of nitrite/nitrate levels and nitric oxide synthase 3 activity. eGcG can also protect endothelial cells via the downregulation of transforming growth factor-β and the Bax/Bcl-2/caspase 3 signaling pathway in the progression of diabetic nephropathy in rats (32,33).…”