Simvastatin Induces Apoptosis And Suppresses Hepatocellular Carcinoma Induced In Rats.

Autor: Elleithi YA; Biochemistry Department, Faculty of Pharmacy, Mansoura University, Mansoura, 3551, Egypt. yomnaelleithi@mans.edu.eg., El-Gayar AM; Biochemistry Department, Faculty of Pharmacy, Mansoura University, Mansoura, 3551, Egypt., Amin MN; Biochemistry Department, Faculty of Pharmacy, Mansoura University, Mansoura, 3551, Egypt.; Biochemistry Department, Faculty of Pharmacy, King Salman International University, Ras Sedr, South Sinai, Egypt.
Jazyk: angličtina
Zdroj: Applied biochemistry and biotechnology [Appl Biochem Biotechnol] 2023 Mar; Vol. 195 (3), pp. 1656-1674. Date of Electronic Publication: 2022 Nov 11.
DOI: 10.1007/s12010-022-04203-0
Abstrakt: Hepatocellular carcinoma (HCC) is a frequent primary aggressive cancer, a crucial cause of cancer-related mortality globally. Simvastatin is a well-known safe cholesterol-lowering medication that has been recently shown to suppress cancer progression. Apoptosis is a well-organized and controlled cellular process that happens both physiologically and pathologically leading to executing cell death. Apoptosis is frequently downregulated in cancer cells. In the present study, we aimed to test the effect of simvastatin on HCC progression. HCC was induced in experimental rats by means of diethylnitrose amine (DEN) and thioacetamide (TAA) injections. Gross examination and liver index along with biochemical analysis of hepatic function were evaluated. Serum alpha-feto protein (AFP) concentration was measured by ELISA. Histopathological examination was used for assessing necroinflammatory scores and fibrosis degree. Apoptosis was assessed using immunohistochemistry (IHC) and quantitative PCR (qPCR). Simvastatin was found to induce apoptosis successfully in HCC and improve liver fibrosis, overall hepatic function, and necroinflammatory score. Simvastatin, therefore, may be a potential adjunctive therapeutic option in clinical settings of treating HCC.
(© 2022. The Author(s).)
Databáze: MEDLINE