Abstract
Liver diseases are one of the most detrimental conditions that may cause inflammation, leading to tissue damage and perturbations in functions. Several drugs are conventionally available for the treatment of such diseases, but the emergence of resistance and drug-induced liver injury remains pervasive. Hence, alternative therapeutic strategies have to be looked upon. Epigallocatechin-3-gallate (EGCG) is a naturally occurring polyphenol in green tea that has been known for its disease-curing properties. In this study, we aimed to evaluate its anti-oxidative potential and protective role against diethylnitrosamine (DEN)-induced liver injury. Four different groups of rats were used for this study. The first group received normal saline and served as the control group. The second group received DEN (50 mg/kg body wt) alone and third group received DEN plus EGCG (40 mg/kg body wt) only. The fourth group were treated with EGCG only. The liver protective effect of EGCG against DEN toxicity through monitoring the alterations in aspartate transaminase (AST), and alanine transaminase (ALT) and alkaline phosphatase (ALP) activities, serum level of pro-inflammatory mediators and anti-oxidant enzymes, histopathological alterations, measurement of cellular apoptosis, and cell cycle analysis was examined. The rats that were given DEN only had a highly significantly elevated levels of liver enzymes and pro-inflammatory cytokines, highly decreased anti-oxidative enzymes, and histological changes. In addition, a significant elevation in the percentage of apoptotic nuclei and cell cycle arrest in the sub- G1 phase was detected. EGCG acts as a hepatoprotectant on DENs by reducing the serum levels of liver functional enzymes, increasing total anti-oxidative capacity, reducing pathological changes and apoptosis, as well as causing the movement of cells from the sub G1 to S or G2/M phase of the cell cycle. In conclusion, EGCG displayed a powerful hepatoprotective additive as it considerably mitigates the liver toxicity and apoptosis induced by DEN.
Highlights
The liver is one of the important organs of our body, having a vital role in the processes of metabolism and detoxification [1]
The aim of the study was achieved through the measurement of liver enzyme levels, levels of pro-inflammatory markers, expression of Phosphatase and tensin homolog (PTEN) protein through immunohistochemistry, and identification of apoptosis by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining
Alterations occur in the transportation function of hepatocytes, triggering
Summary
The liver is one of the important organs of our body, having a vital role in the processes of metabolism and detoxification [1]. Around 10% of the world population is oppressed by liver disease [2]. Chronic hepatitis, and hepatocellular carcinoma are some of the most comprehensive and colloquial liver diseases, drawing considerable attention from medical professionals and scientists [3,4]. A large number of pro-inflammatory cytokines are released from injured cells, which stimulate cells, such as Kupffer cells, to deliver more inflammatory mediators and various types of free radicals. This signal is further amplified by the recruitment of neutrophils to the site of injury.
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