Epigallocatechin-3-gallate protects against cisplatin-induced nephrotoxicity by inhibiting endoplasmic reticulum stress-induced apoptosis

Abstract

Cisplatin (CP)-induced nephrotoxicity hampers its application in clinic. Green tea, particularly its predominant polyphenolic constituent epigallocatechin-3-gallate (EGCG), possesses anti-inflammatory, antioxidant, and anti-apoptotic properties. The present study was designed to investigate the protective effects of EGCG against CP-induced nephrotoxicity in mice. Male C57/BL6 mice in different groups received single injection of CP (20 mg/kg) and EGCG (100 mg/kg) in various sets and kidney tissues and blood were collected after killing. Then, samples were used for biochemical and immunohistochemical assay. Our results showed EGCG decreased biochemical factors and immunohistochemical damage induced by CP. Besides, expression of phosphorylatedextracellular signal-regulated kinase (p-ERK), glucose-regulated protein 78 (GRP78), caspase-12, and apoptosis of kidney were decreased by EGCG via inhibition of endoplasmic reticulum (ER) stress-induced apoptosis.

Natural polyphenols prevent indomethacin-induced and diclofenac-induced Caco-2 cell death by reducing endoplasmic reticulum stress regardless of their direct reactive oxygen species scavenging capacity

“…These three polyphenols (i.e. EGCG, QUE and RUT) were reported for their activity in preventing tissue damages from ER stressors such as cisplatin, MPP + , tunicamycin, A23187 and thapsigargin . For example, EGCG was able to prevent cisplatin‐mediated nephrotoxicity .…”

“…EGCG, QUE and RUT) were reported for their activity in preventing tissue damages from ER stressors such as cisplatin, MPP + , tunicamycin, A23187 and thapsigargin. [44][45][46][47] For example, EGCG was able to prevent cisplatin-mediated nephrotoxicity. [44] QUE suppressed ER stress responses in intestinal LS180 and Caco-2 cells exposed to tunicamycin, A23187 and thapsigargin.…”

“…[44][45][46][47] For example, EGCG was able to prevent cisplatin-mediated nephrotoxicity. [44] QUE suppressed ER stress responses in intestinal LS180 and Caco-2 cells exposed to tunicamycin, A23187 and thapsigargin. [46,47] In addition, RUT could prevent neuronal SH-SY5Y cells death via inhibition of ER stress relating to MPP + treatment.…”

Epigallocatechin‐3‐Gallate Inhibits Ethanol‐Induced Apoptosis Through Neurod1 Regulating CHOP Expression in Pancreatic β‐Cells

“…Asaumi et al () demonstrated that EGCG suppressed the activation of pancreatic stellate cells induced by ethanol through the antioxidative effect. Several studies demonstrated that EGCG inhibited ER stress‐induced apoptosis (Wu et al, ; Chen et al, ). However, whether EGCG had effect on the damage of ethanol‐induced β ‐cells remains unclear.…”

The Green Tea Polyphenol(—)-epigallocatechin-3-gallate and its beneficial roles in chronic kidney disease

“…First, the imbalance in ER homeostasis, as multifunctional organelle, caused disturbance of calcium homeostasis, glucose deprivation, increasing of ROS formation and oxidative stress induction [45] . Chen et al showed that EGCG decreased p-ERK, GRP78, caspase-12 of kidney, as ER stress-related markers via inhibition of ER stress-induced apoptosis [46] . Second, a recent study has examined the effect of protection again cisplatin induced renal injury by EGCG through mitochondrial protection by improving mitochondrial electron chain complexes, mitochondrial antioxidant function in enzymes MnSOD and GPX, and improving cisplatin-induced mitochondrial oxidative/nitrative damage and anti-inflammatory effect [37] .…”