ATRA modulates gluconeogenesis and triglyceride biosynthesis pathway of liver in elastase induced emphysematous rats
Emphysema is a chronic pulmonary disorder characterized by the destruction and enlargement of the gas exchanging units known as alveoli. Chronic inflammation is one of the critical features associated with pathogenesis of emphysema. The inflammatory mediators generated during emphysema are thought to be infiltrated into the circulatory system, leading to systemic inflammation and thus, affecting other vital organs. The potential role of ATRA, an anti-inflammatory bio-molecule, towards molecular mechanisms governing systemic inflammation due to inflammatory mediator’s overspills in emphysema is poorly understood. Therefore, the present study deals with investigating the potential effect of ATRA on physiological functions of liver tissue in an established elastase induced emphysema rat model. Three experimental groups (i.e., control, SS; emphysema, ES; and therapy, EA) were prepared. Subsequently, liver from each rat was collected for elastase activity assay, histopathology, real-time PCR based mRNA expression analyses, total lipid estimation and western blot analysis. ATRA supplementation in emphysema group decreases elastase activity. Liver histopathology photomicrographs clearly shows an increase in number of Kupffer cells in ES than SS, while, a decrease in number of Kupffer cells was found in EA. Furthermore, upon validation at mRNA and protein level, expressions of TNF-α, enzymes of gluconeogenesis and triglyceride biosynthesis pathway were significantly increased in ES while decreased in EA when compared to SS. Therapeutic supplementation of ATRA posed a beneficial effect in maintaining the normal architecture of liver tissue along with modulation of gluconeogenesis and triglyceride biosynthesis pathways.