# Antioxidant and Biological Activities of Mahajanaka Mango Pulp Extract in Murine Models
## 4 Discussion
However, it is essential to note that the anti-inflammatory activity of MPE, like other NSAIDs, may not be suitable for use in the early stages of peptic ulcer occurrence since it may inhibit the function of prostaglandandins, which can help to suppress HCl secretions in the stomach. Further studies should be conducted to investigate the underlying mechanisms of MPE for the treatment of peptic ulcers at higher doses. Liver injury refers to the impairment of liver function and structure, which can be caused by a variety of factors including viral infections and alcohol consumption, and can be attributed to the use of certain medications such as CCl4 and paracetamol [57; 58]. In the present study, we investigated the effect of MPE on CCl4- and paracetamol-induced liver injuries in rat models. CCl4 is metabolized by the liver into a highly reactive free radical called trichlothermethyl radical (\({}^{\bullet}\)CCI3), while paracetamol, which is also known as acetaminophen, undergoes metabolism via the cytochrome P450 pathway leading to the production of N-acetyl-p-benzoquinone imine (NAPQI), a highly reactive and toxic metabolite [59; 60]. Both of these can cause oxidative stress, inflammation, and lipid accumulation in the liver, ultimately resulting in hepatic steatosis and liver damage [61]. Indeed, liver damage causes a leakage of liver enzymes including AST, ALT, and alkaline phosphatase (ALP). Our present study demonstrated that the administration of MPE at 250 mg/kg BW effectively reduced levels of ALT and fat deposits in rats with both CCl4- and paracetamol-induced hepatotoxicity. It is likely that the hepatotoxicity effects of MPE containing mangiferin may be attributed to its ability to scavenge lipid radicals and consequently reduce fat deposits. This hypothesis is supported by the outcomes of previous studies that reported the hepatotoxicity effects of mangiferin isolated from mango bark by reducing the levels of ALP, ALT, triglycerides, total cholesterol, and lipid peroxidation while increasing reduced glutathione (GSH) in rats with galactosamine-induced liver damage [62]. Another previous study found that the administration of mangiferin also improved LPS- and D-galactosamine-induced acute liver injuries in mice via suppression of the levels of serum ALT, AST, IL-1\(\beta\), and TNF-\(\alpha\), as well as hepatic malondialdehydehyde (MDA) and reactive oxygen species (ROS) levels [63]. Additionally, mangiferin potently reduced fat accumulation, as well as the number of Kupffer cells and the expression of nuclear factor kappa B (NF-kB), in the livers and adipose tissues of high-fat diet (HFD)-induced metabolic mice [64]. Furthermore, [PERSON] et al. demonstrated that \(\beta\)-carotene significantly improved paracetamol-induced liver damage in rats by reducing the levels of AST, while increasing superoxide dismutase (SOD), catalase, and GSH activities [65]. Another study found that vitamin C also protected against paracetamol-induced hepatotoxicity in rats by ameliorating the levels of ALT, AST, and lipid peroxidation [66]. These data are consistent with the antioxidant and anti-inflammatory activities of mangiferin, \(\beta\)-carotene, and vitamin C in MPE. These findings suggest that MPE, containing mangiferin, \(\beta\)-carotene, and vitamin C, has the potential to protect the liver against CCl4- and paracetamol-induced liver injuries by reducing liver enzymes and fat deposits. Taken together, these findings indicate that Mahajanaka mango, containing mangiferin, \(\beta\)-carotene, and vitamin C, possesses a positive protective effect against oxidative stress, pain, inflammation, gastric ulceration, and hepatotoxicity. The results of this study provide supportive evidence for the antioxidant, analgesic, anti-inflammatory, gastroprotective, and hepatotoxicity properties of Mahajanaka mango, which could be an effective agent against oxidative stress and inflammation-associated diseases.