Eremomastax speciosa extract mitigates cadmium-induced hepato- and cardiotoxicity in rats by modulating PXR, LRH-1, FXR genes, inflammatory markers, troponin, and liver enzymes
摘要
Cadmium chloride (CdCl₂) exposure presents significant health hazards, particularly hepatotoxicity, with secondary effects on cardiac function. This study evaluates the protective effects of Eremomastax speciosa extract against CdCl₂-induced hepato- and cardiotoxicity in rats by examining key molecular and biochemical markers. Rats were exposed to CdCl₂ (5 mg/kg body weight) for 21 days to induce toxicity. Cadmium exposure resulted in a notable increase in liver and kidney somatic indices, elevated serum liver enzymes, inflammatory cytokines, cardiac troponin, and upregulated mRNA expression of the nuclear receptors Farnesoid X Receptor (fxr), Pregnane X Receptor (pxr), and Liver Receptor Homolog-1 (lrh-1). Electrolyte imbalances and histopathological changes, including vascular congestion, inflammation, and disrupted hepatocyte structure, were also observed. Concurrent administration of E. speciosa extract significantly mitigated these toxic effects, normalizing liver enzyme levels, reducing inflammation, and restoring hepatic architecture. The findings suggest that E. speciosa extract exerts potent protective effects against cadmium-induced hepatotoxicity, likely through modulation of nuclear receptor pathways (fxr, pxr, and lrh-1), inflammatory responses, and cardiac injury markers. This highlights its therapeutic potential for preventing both hepatic and cardiac damage in cadmium exposure.