HBP Surgery Week 2024

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[E-poster - Liver (Liver Disease/Surgery)]

[EP 058] Solid Lipid Nanoparticle Ganodric acid ameliorates the High fat induced Nonalcoholic fatty liver disease via alteration Gut Microbiota and PI3K/AKT/mTOR Signaling pathway
Deeksha Chauhan1, Vikas Kumar2
Department of Hepatobiliary and Pancreatic Surgery, Rajkamal Science Management College, Department of Liver Transplantation and Hepatobiliary Surgery, SIHAS

Background : Nonalcoholic fatty liver disease (NAFLD) is a condition characterized by the accumulation of fat in the liver. NAFLD is considered a spectrum of liver conditions, ranging from simple fatty liver (steatosis) to a more severe form called nonalcoholic steatohepatitis, which can progress to cirrhosis and, in some cases, hepatocellular carcinoma (HCC), most common type of primary liver cancer. In this study, we fabricated the solid lipid nanoparticle (SLN) of ganodric acid (GA) and scrutinized the chemoprotective effect against high fat diet (HFD) and Diethylnitrosamine (DEN) induced NAFLD in rats.

Methods : Double emulsion solvent displacement model was used for the preparation of SLN-GA. Intraperitoneal administration of DEN (100 mg/kg) was used for the induction of HCC in rats for 2 weeks. The rats were divided into 2 groups and received the HFD with or without treatment with SLN-GA for 20 weeks. Body weight, tumor incidence, tumor nodules, hepatic, non-hepatic, apoptosis, antioxidant, pro-inflammatory and inflammatory were estimated. For the determination of gut microbiota, we collected the stools of all rats.

Results : Surface methodology showed the particle size (174.3 nm) and polydispersity index (0.228) for SLN-GA. SLN-GA remarkably suppressed tumor nodules, tumor incidence and average size nodules. SLN-GA remarkably decreased the level of AFP, ALT, AST, ALP, GGT; non-hepatic parameters viz., bilirubin, total protein, respectively. SLN-GA also suppressed the level of SOD, GSH, GPx, CAT and boosted the level of LPO. SLN-GA significantly (P<0.001) suppressed the level of inflammatory cytokines like TNF-α, IL-1β, IL-6; inflammatory parameters such as COX-2, PGE2, VEGF, iNOS and NF-κB, respectively. SLN-GA significantly (P<0.001) altered the expression of Erbb2, Pik3rl, PIk3ca, Akt1 and Map3k1, respectively. Moreover, SLN-GA enhanced gut microbial richness and diversity and altered the relative abundance of firmicutes and bactericides, respectively.

Conclusions : SLN-GA remarkably suppressed the HFD-induced NAFLD in rats via alteration of gut microbiota and PI3K/AKT/mTOR Signaling pathway.



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E-poster
E-Session 03/21 ALL DAY