A Comprehensive Review of Experimental Animal Models of Hepatopathy

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Abstract

At this moment, liver dysfunction is a major source of destruction, and its widespreadity is accentuated in the developed republics. The liver is an imperative organ of the body and is involved in metabolism and regulation. The large number of medications, toxins, and plant-derived products has been claimed to cause liver dysfunction, which is potentially life intimidating to humans. Currently, there is a shortfall in encouraging treatment for treating patients with liver dysfunction due to the nonexistence of empathy for gesturing offenders serviceable in the pathogenesis of liver toxicity. Hepatic dysfunction is manifested by hepatic karyopyknotic, eosinophilic or acidophilic cell plasm, followed by excessive steatosis, liver injury, and oxidative degradation of lipids that cause centrilobular necrosis in hepatocytes. Different signaling mechanism, like activation of Kupffer cells, NK cells, inflammatory mediators, and ROS are associated with the pathogenesis of liver dysfunction. A good empathy of chief mechanisms is prerequisite for the scheming of novel curative medications. Consequently, animal models are being developed to impressionist hepatic ailments. From the several decades, researchers are using distinctive animal models for discovering and understanding pathogenesis of hepatic ailments and associated abusiveness. This current review has been framed to discuss numerous new and traditional experimental models for hepatotoxicity studies. Numerous animal models have been evolved to evaluate the pathogenesis and develop drugs for hepatotoxicity. Experimental modes of hepatotoxicity are influential for invention of novel molecular signaling trails for the improvement of human health.

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Gupta, R. K., Chaudhary, S., El-Shorbagi, A. N., Sara, U. S., Shukla, P., Swain, S. R., … Murthy, P. N. (2022). A Comprehensive Review of Experimental Animal Models of Hepatopathy. Biomedical and Pharmacology Journal. Oriental Scientific Publishing Company. https://doi.org/10.13005/bpj/2397

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