Detailed Abstract
[E-poster - Liver (Liver Disease/Surgery)]
[EP 015] Chemoprotective effect of Crocetin-Dextrin nano-formulation against N-diethylnitrosamine induced Hepatocellular Carcinoma in Wistar rats via mitochondrial apoptosis, antioxidative, anti-inflammatory and PI3K/Akt/mTOR signaling pathways
Vikas Kumar1, Firoz Anwar2
Department of Hepatobiliary and Pancreatic Surgery, Sam Higginbottom University of Agriculture, Technology & Sciences, Department of Biochemistry & Molecular Biology, King Abdulaziz University
Background : Hepatocellular carcinoma (HCC) is known to have a high prevalence, particularly in regions with a high incidence of chronic liver diseases such as hepatitis B and C infections, alcoholic liver disease, and non-alcoholic fatty liver disease. In this study, we fabricate the crocetin-dextrin nano-formulation (CDNF) against N-diethylnitrosamine (DEN) induced hepatic cancer in rats.
Methods : Crocetin-Dextrin nano-formulation was prepared the aqueous nano-emulsion of crocetin and dextrin. The Wistar rats divided into different groups and DEN (200 mg/kg) were for the induction of HCC in rats and received the oral administration of crocetin and CDNF for 20 weeks. The microscopical study was carried out for the confirmation of hepatic nodules. Liver indices like Alpha feto protein (AFP), aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), albumin, bilirubin, total protein, C-reactive protein (CRP); oxidant parameters activity along with nitric oxide (NO); inflammatory cytokines; inflammatory parameters levels were estimated. The level of AKT, mTOR, Bax, p-53, Bcl-2, caspase-3 and PI3K gene were estimated.
Results : CDNF treatment remarkably reduced the tumor size, average size of nodules and tumor nodules. CDNF also reduced the body weight and suppressed the level of AFP, AST, ALT, ALP, albumin, bilirubin, total protein and CRP level. CDNF also altered the level of antioxidant parameters like MDA, GPx, GSH, CAT and NO level. CDNF significantly (P<0.001) reduced the level of TNF-α, IL-1β, IL-6 and improved the level of IL-10. CDNF also suppressed the level of inflammatory parameters viz., COX-2, PGE2, VEGF and iNOS, respectively. CDNF also altered the level of gene expression like AKT, mTOR, Bax, p-53, Bcl-2, caspase-3 and PI3K. Histopathological observation suggest that CDNF treated rats exhibited the less necrosis, inflammatory cells.
Conclusions : The result suggests that CDNF was able to alter the HCC in the rats via regulation of Bax/Bcl-2/p53 and PI3K/Akt/mTOR signaling pathways.
Methods : Crocetin-Dextrin nano-formulation was prepared the aqueous nano-emulsion of crocetin and dextrin. The Wistar rats divided into different groups and DEN (200 mg/kg) were for the induction of HCC in rats and received the oral administration of crocetin and CDNF for 20 weeks. The microscopical study was carried out for the confirmation of hepatic nodules. Liver indices like Alpha feto protein (AFP), aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), albumin, bilirubin, total protein, C-reactive protein (CRP); oxidant parameters activity along with nitric oxide (NO); inflammatory cytokines; inflammatory parameters levels were estimated. The level of AKT, mTOR, Bax, p-53, Bcl-2, caspase-3 and PI3K gene were estimated.
Results : CDNF treatment remarkably reduced the tumor size, average size of nodules and tumor nodules. CDNF also reduced the body weight and suppressed the level of AFP, AST, ALT, ALP, albumin, bilirubin, total protein and CRP level. CDNF also altered the level of antioxidant parameters like MDA, GPx, GSH, CAT and NO level. CDNF significantly (P<0.001) reduced the level of TNF-α, IL-1β, IL-6 and improved the level of IL-10. CDNF also suppressed the level of inflammatory parameters viz., COX-2, PGE2, VEGF and iNOS, respectively. CDNF also altered the level of gene expression like AKT, mTOR, Bax, p-53, Bcl-2, caspase-3 and PI3K. Histopathological observation suggest that CDNF treated rats exhibited the less necrosis, inflammatory cells.
Conclusions : The result suggests that CDNF was able to alter the HCC in the rats via regulation of Bax/Bcl-2/p53 and PI3K/Akt/mTOR signaling pathways.
SESSION
E-poster
E-Session 03/21 ALL DAY