Exploring the Mechanisms of Lipopolysaccharide-Induced Liver Damage in a Rat Model

Liver injury is closely associated with changes in gut microbiota, leading to the release of bacterial endotoxins such as lipopolysaccharide (LPS). These endotoxins interact with toll-like receptors (TLRs), especially TLR4, expressed on liver immune cells. Although LPS is known to play a crucial role in liver pathogenesis, the progression of liver dysfunction following LPS exposure remains insufficiently explored. This study aimed to develop and characterize a rat model of LPS-induced liver injury. Animals were divided into five groups (n=6). Group I received saline (control), Group II received alcohol (1.24%, 0.4 ml), and Groups III–V were sensitized with increasing doses of LPS (1 μg, 10 μg, and 100 μg/rat, i.p.) for 10 days and challenged on day 21, with LPS (10 μg/rat, i.p.) which markedly increased the liver parameters. Biochemical parameters like SGPT, SGOT, ALP, bilirubin, total protein, globulin, and albumin were evaluated at multiple time points. Groups III and IV showed significant increased in AST, ALT and ALP level. The protein levels were significantly reduced in alcohol treated group. Bilirubin level was significantly increased in LPS treated and alcohol treated groups around 28th day of treatment, which indicates liver injury. This model demonstrates a reproducible method to study LPS-induced liver damage.