Mechanistic Insights into Oxidative Stress and Apoptosis Mediated by Tannic Acid in Human Liver Hepatocellular Carcinoma Cells.

Rene B Khan,Daniel G Amoako,Hezekiel M Khumalo,Priscilla Mhlanga,Pearl O Perumal,Anou M Somboro

doi:10.3390/ijms20246145

Rene B Khan, Daniel G Amoako + Show 4 more

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https://doi.org/10.3390/ijms20246145

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Abstract

The study investigated the cytotoxic effect of a natural polyphenolic compound Tannic acid (TA) on human liver hepatocellular carcinoma (HepG2) cells and elucidated the possible mechanisms that lead to apoptosis and oxidative stress HepG2 cell. The HepG2 cells were treated with TA for 24 h and various assays were conducted to determine whether TA could induce cell death and oxidative stress. The cell viability assay was used to determine the half maximal inhibitory concentration (IC50), caspase activity and cellular ATP were determined by luminometry. Microscopy was employed to determine deoxyribonucleic acid (DNA) integrity, while thiobarbituric acid (TBARS) and nitric oxide synthase (NOS) assays were used to elucidate cellular reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. Western blotting was used to confirm protein expression. The results revealed that tannic acid induced caspase activation and increased the presence of cellular ROS and RNS, while downregulating antioxidant expression. Tannic acid also showed increased cell death and increased DNA fragmentation. In conclusion, TA was able to induce apoptosis by DNA fragmentation via caspase-dependent and caspase-independent mechanism. It was also able to induce oxidative stress, consequently contributing to cell death.

Highlights

Cancer is one of the leading causes of death worldwide with a high mortality rate, which makes it an imperative public health issue [1]
The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was used to measure Tannic acid (TA) toxicity after a 24 h of exposure to human liver hepatocellular carcinoma (HepG2) cells; this was to provide a preliminary data showing that TA could inhibit the metabolic activity and respiratory potential of the liver HepG2 cells at the concentrations used
This study focused on investigating the interaction of TA and specific liver cancer cells (HepG2) to provide insights into the mechanism by which TA leads to cell death

Summary

Introduction

Cancer is one of the leading causes of death worldwide with a high mortality rate, which makes it an imperative public health issue [1]. Environmental and lifestyle factors, including smoking, diet, and lack of exercise, cause 90% of all cancers. Liver cancer has a steadily increasing mortality rate at 8.2% of all cancer-caused death worldwide [2]. It has a poor prognosis of about 31% for people with localised liver cancer from different histological groups. Liver cancer ranges from hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA) to mixed hepatocellular cholangiocarcinoma (HCCCCA), fibrolamellar HCC (FLC), and the paediatric neoplasm hepatoblastoma [3,4]. The most common primary liver cancers are HCC and iCCA, while others, such as mixed HCC-CCA tumor, account for less than 1% [5]

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