LIPOPOLYSACCHARIDE (LPS) AND MURAMYL DIPEPTIDE (MDP) INDUCED CHRONIC LIVER INJURY IN HIGH FAT DIET FED RAT–A POSSIBLE MODEL FOR NON ALCOHOLIC FATTY LIVER DISEASEAbstract
Liver defend the PAMPs or DAMPs via regulation of innate immunity through modulation of “TOLL LIKE RECEPTORS and NOD LIKE RECEPTORS” A breakdown of tolerance may induce in appropriate immune response leads to acute and chronic liver diseases like NASH/NAFLD thus considered as disorders of immune response. HFD is itself a basic component for generating metabolic disorders and major source for formation of endotoxins in body through leaky gut and sensitization of the TLR4. NAFLD is one of the groups of disease which links the innate immunity through the metabolic disorder. Agonist of TLR4 – LPS is the primary and NLRP3 agonist MDP is secondary signal transducer for the sensitization of the Caspase activation cascade and TNFα activation serves as the proinflammatory cytokines in disease like NAFLD. The present study was elucidated to develop combinations of Lipopolysaccharide and Muramyl dipeptide induced experimental model of NAFLD in HDF fed rats. Various parameters such as body weight, SGOT, SGPT, ALP, Direct Billirubin, serum triglyceride, weight of liver, and ratio of liver weight to body weight were done at the end of study. The established model was statistically evaluated by measuring significant changes in these parameters. The outcome of the study was found that the MDP alone is also a trigger for the development of NAFLD.