(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice

Abstract

Background/Aims: Exposure to arsenic in individuals has been found to be associated with various health-related problems including skin lesions, cancer, and cardiovascular and immunological disorders. (-)-Epigallocatechin-3-gallate (EGCG), the main and active polyphenolic catechin present in green tea, has shown potent antioxidant, anti-apoptotic and anti-inflammatory activity in vivo and in vitro. Thus, the present study was conducted to investigate the protective effects of EGCG against arsenic-induced inflammation and immunotoxicity in mice. Methods: Serum IL-1β, IL-6 and TNF-α were determined by ELISA, tissue catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide and caspase 3 by commercial kits, mitochondrial membrane potential with Rh 123, mitochondrial ROS with 2’,7’-dichlorofluorescin diacetate (DCFH-DA), apoptotic and necrotic cells and T-cell phenotyping with Flow cytometry analysis. Results: The results showed that arsenic treatment significantly increased oxidative stress levels (as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione and reactive oxygen species), increased levels of inflammatory cytokines and promoted apoptosis. Arsenic exposure increased the relative frequency of the CD8+(Tc) cell subpopulation (from 2.8 to 18.9%) and decreased the frequency of CD4+(Th) cells (from 5.2 to 2.7%). Arsenic exposure also significantly decreased the frequency of T(CD3) (from 32.5% to 19.2%) and B(CD19) cells (from 55.1 to 32.5%). All of these effects induced by NaAsO₂ were attenuated by EGCG. Conclusions: The present in vitro findings indicate that EGCG attenuates not only NaAsO₂-induced immunosuppression but also inflammation and apoptosis.

Epigallocatechin gallate improves airway inflammation through TGF‑β1 signaling pathway in asthmatic mice

“…It has been found that EGCG can affect apoptosis, autophagy or (and) block the flow of calcium ions in cells, which achieve anti-inflammatory and anti-apoptotic effects ( 28 – 30 ). The present study showed that EGCG could mitigate OVA-mediated airway inflammation in mouse models of asthma, which was consistent with the results of the study by Yu et al ( 31 ).…”

Silver nanoparticles have lethal and sublethal adverse effects on development and longevity by inducing ROS-mediated stress responses

“…Mechanistically, we show that ingestion of AgNPs during the larval stage leads to caspase-3-dependent apoptosis and double-stranded DNA breaks in multiple larval tissues. However, it cannot be concluded that such cytotoxic responses are directly attributable to AgNPs because several lines of research have suggested that the ROS generated and the dissolved silver ions may contribute to the tissue-wide occurrence of apoptosis and DNA damage 74 – 78 .…”

Epigallocatechin‐3‐gallate partially restored redox homeostasis in arsenite‐stressed keratinocytes

“…EGCG was reported to protect human umbilical vein endothelial cells from PM 2.5 ‐induced oxidative stress injury by upregulating Nrf2/HO‐1 via activation of the p38, mitogen‐activated protein kinases and the extracellular signal‐regulated protein kinases 1 and 2 (ERK1/2) signaling pathways (Yang et al, ). EGCG has been associated with attenuation of AsIII‐induced oxidative stress, inflammation, immune suppression and apoptosis in Balb/c mice (Yu et al, ). EGCG also prevented AsIII‐mediated hepatotoxicity by activating Nrf2 pathway in Chang human hepatocyte cells and albino male Sprague–Dawley rats (Han et al, ).…”

“…On the other hand, EGCG has been reported with Nrf2 inducing activity in in vitro and in vivo systems (Dong et al, ; Zhang, Wu, Sang, & Ruan, ). EGCG has also demonstrated protective effects against arsenic‐induced oxidative stress in mice (Yu, Pei, Huang, & Li, ) and cardiotoxicity in rats (Sun et al, ).…”