## 4 Discussion  
The current study results provide evidence of the role of EGCG in the regulation of apoptosis, antioxidant production, and inflammatory cytokines in rat liver damage with the concept of mitochondrial homeostasis. Significantly, the current study results also advocate for an argument for further analysis of EGCG or structurally related molecules as inhibitors of TNF-\(\alpha\) and IL-6 synthesis and possibly other cytokine-regulated diseases. The anti-inflammatory, tumor-suppressing, and anti-oxidative effects of EGCG have been studied formerly. Howbeit, its antioxidant effect is the most imperative one [26; 27]. During liver injury, the generation of free radicals and reactive oxygen species plays a critical role in the augmentation of tissue damage. As the injury proceeds, inflammatory cascades are activated, leading to the release of pro-inflammatory cytokines and free radicals, which finally causes activation of inflammatory Kupffer cells and recruitment of neutrophils at the site of injury. Stimulated inflammatory cells are accountable for the generation of more free radicals and provoked secretion of pro-inflammatory mediators. A large amount of released free radicals induce lipid peroxidation in the cellular phospholipid bilayer, which can damage the cytosol and other cellular organelles [5]. Thoughfully, the anti-oxidative effects of EGCG come into action through activation of anti-oxidation protective signaling, thus reducing injury [28; 29]. Similarly, other studies have shown anti-oxidative and preventive effects of EGCG on different hepatic injury animal models [30; 31]. In the current study, DEN-induced liver injury in a rat model was characterized by an increase in the secretion of pro-inflammatory cytokines, including IL-6 and TNF-\(\alpha\). This study shows that EGCG ameliorated liver injury along with a decrease of IL-6 and TNF-\(\alpha\) levels in serum. These results are supported by previous studies in which IL-6 deficiency or IL-6R blockade ameliorated hepatocyte damage, indicating that the control of IL-6 production may produce a valuable outcome in liver injury [32; 33]. A previous study by [PERSON] et al. [34] showed that administration of green tea polyphenols showed a role in the prevention of acute liver injury in mice by reducing CRP, IL-6,  
Figure 9: **Cell cycle significance analysis between the groups using a bar diagram**. Relative frequencies of cells in different phases of the cell cycle in (**a**) control, (**b**) DEN only-treated, (**c**) DEN + EGCG-treated, and (**d**) EGCG only-treated groups. and TNF-\(\alpha\). However, this study specifically provides insight into one of the potential mechanisms of EGCG's liver protective activity. Moreover, EGCG treatment also increases the levels of anti-oxidative enzymes SOD, CAT, and GPx, suggesting the activation of anti-oxidation protective signaling pathways to provide protection against oxidative damage. The upregulation of serum levels of AST, ALP, and ALT is a strong indication of the manifestation of oxidative stress in DEN-induced liver injury. The current study result demonstrates that EGCG reduces oxidative stress by reducing the serum levels of these liver functionality enzymes. It has been reported that oxidative stress regulates the apoptotic signaling pathway in cells. This result agrees with a previous finding that treatment with EGCG plays a significant role in the reduction of liver injury, oxidative stress, and the inflammatory response [5]. Moreover, EGCG also significantly attenuated the severity of CCI (4)-induced liver injury and the progression of liver fibrosis. Another study reported that in vitro model of oxidative stress induced by ethanol provided evidence that EGCG prevented some aspect of liver cell injury caused by ethanol [35]. _PTEN_ is one of the tumor suppressor genes and it is located in the 10q23 region encoding for a 403-amino acid multifunctional protein that comprises lipid and protein phosphatase activities [36].