BIOCHEMICAL AND HISTOLOGICAL ASSESSMENT OF MELOXICAM ON LIVER TOXICITY IN WISTAR RATS

agents for the management of pain, fever, and inflammation. Despite their proven clinical value, several NSAIDs have been implicated in hepatic dysfunction and oxidative stress when used chronically or at high doses. The liver, being the primary organ for xenobiotic metabolism, is particularly vulnerable to drug-induced toxicity due to the generation of reactive metabolites and free radicals during biotransformation processes. Meloxicam, an enolic acid derivative of the meloxicam class of NSAIDs, is a preferential cyclooxygenase-2 (COX-2) inhibitor commonly prescribed for musculoskeletal disorders, arthritis, and postoperative pain. Although it is considered relatively safer than non-selective NSAIDs, reports of hepatocellular injury associated with meloxicam therapy warrant further investigation into its potential hepatotoxicity at varying exposure levels. This research is therefore designed to evaluate the biochemical and histological effects of meloxicam on the liver of adult male Wistar rats. A total of twenty healthy male Wistar rats, weighing between 180g–300g, were randomly assigned into six experimental groups of four animals each. The groups received graded oral doses of meloxicam, low dose, high dose, low dose meloxicam and vitamin C, high dose meloxicam and vitamin C, vitamin C only once daily for forty-five days while the control group received an equivalent. At the end of the treatment period, animals were sacrificed, and blood samples collected for serum biochemical analyses of liver function biomarkers such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP). In addition, hepatic tissues were fixed and processed for histopathological examination using hematoxylin and eosin (H&E) staining to assess cellular integrity, inflammatory infiltration, vascular congestion, and degenerative changes. Data were statistically analyzed using one-way analysis of variance (ANOVA), followed by appropriate post-hoc tests, with results expressed as mean ± standard error of mean (SEM) and significance set at p < 0.05. It is seen that meloxicam administration, particularly at higher doses, resulted in dose-dependent elevations of hepatic enzyme levels, disruption of redox balance, and histological evidence of hepatocellular damage. These outcomes suggested oxidative stress as a key mechanism in meloxicam-induced hepatic injury. This research aims to provide insight into the hepatic safety profile of meloxicam, establish a link between biochemical alterations and histological manifestations, and contribute to the understanding of drug-induced hepatotoxicity associated with prolonged or high-dose NSAID therapy. This research will be valuable for clinicians and pharmacologists in ensuring safer therapeutic use of meloxicam and other related NSAIDs.