Cleistocalyx nervosum var. paniala berry extract and cyanidin‐3‐glucoside inhibit hepatotoxicity and apoptosis

Author:

Panritdum Pasitta1,Muangnoi Chawanphat2,Tuntipopipat Siriporn2,Charoenkiatkul Somsri3,Sukprasansap Monruedee4ORCID

Affiliation:

1. Graduate student in Master of Science Program in Nutrition, Faculty of Medicine Ramathibodi Hospital and Institute of Nutrition Mahidol University Bangkok Thailand

2. Cell and Animal Model Unit, Institute of Nutrition Mahidol University Nakhon Pathom Thailand

3. Institute of Nutrition Mahidol University Nakhon Pathom Thailand

4. Food Toxicology Unit, Institute of Nutrition Mahidol University Nakhon Pathom Thailand

Abstract

AbstractExcessive oxidative toxicity in liver cells is a significant risk factor that can cause cellular injury, leading to the development of chronic liver disease (CLD). Natural anthocyanins have been shown to prevent the harmful effects of oxidative toxicity in mammalian cells. Ripe Cleistocalyx nervosum var. paniala berry fruits are rich in anthocyanins, which have been reported to possess many health benefits. Therefore, this study examined the protective effect of ethanolic fruit extract of C. nervosum var. paniala (CNPE) against hydrogen peroxide (H2O2)‐induced oxidative damage and cell death in human hepatoma HepG2 cells. Results showed that CNPE had strong antioxidant capabilities and high amounts of total phenolics and anthocyanins. HPLC analysis showed that CNPE consists of cyanidin‐3‐glucoside (C3G). Our investigations found that HepG2 cells pretreated with CNPE or anthocyanin C3G inhibited H2O2‐induced cellular damage and apoptosis by increasing the viability of cells, the expression of antiapoptotic Bcl‐2 protein, and the activities of cellular antioxidant enzymes, namely SOD, CAT, and GPx. Moreover, both CNPE and C3G significantly suppressed expression of apoptotic proteins (Bax and cytochrome c) and the activities of cleaved caspase‐9 and caspase‐3 caused by H2O2. Our results indicate that CNPE and C3G can suppress H2O2‐induced hepatotoxicity and cell death through stimulation of endogenous antioxidant enzyme activities and inhibition of apoptosis pathway in HepG2 cells. These findings might support development of CNPE as an alternative natural product for preventing CLD.

Funder

National Research Council of Thailand

Publisher

Wiley

Subject

Food Science

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