Silibinin treatment results in reducing OPA1&MFN1 genes expression in a rat model hepatic ischemia–reperfusion

• Published in: Molecular biology reports Vol. 47; no. 5; pp. 3271 - 3280
• Main Authors: Qajari, Neda Masoumi, Shafaroudi, Majid Malekzadeh, Gholami, Milad, Khonakdar-Tarsi, Abbas
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01.05.2020; Springer Nature B.V
• Subjects: Animal Anatomy; Animal Biochemistry; Animals; Apoptosis; Apoptosis - drug effects; Atrophy; Biomedical and Life Sciences; Cell death; Degeneration; Disease Models, Animal; Electron microscopy; Gene expression; Gene Expression - drug effects; Gene Expression - genetics; Gene Expression Regulation - drug effects; Gene Expression Regulation - genetics; GTP Phosphohydrolases - genetics; GTP Phosphohydrolases - metabolism; Hepatocytes; Histology; Ischemia; Ischemia - pathology; Laparotomy; Life Sciences; Liver; Liver - metabolism; Male; Membrane Proteins - genetics; Membrane Proteins - metabolism; Mitochondria; Mitochondria - metabolism; Mitochondrial Dynamics - genetics; Mitochondrial Membranes - drug effects; Mitochondrial Membranes - metabolism; Mitochondrial Proteins - genetics; Mitochondrial Proteins - metabolism; Morphology; Original Article; Rats; Rats, Wistar; Reperfusion; Reperfusion Injury - drug therapy; Reperfusion Injury - metabolism; Serum levels; Silibinin; Silybin - metabolism; Silybin - pharmacology; Reperfusion; Ischemia; Fusion; Silibinin
• ISSN: 0301-4851; 1573-4978
• DOI: 10.1007/s11033-020-05383-w

The mitochondrial damage has a pivotal role in triggering apoptosis and cell death. This study assessed the effect of silibinin on optical atrophy-1 (OPA1) and mitofusin-1 (MFN1) gene expression in liver tissue during hepatic warm ischemia–reperfusion (IR). Four groups of rats, eight rats each were designed: Vehicle: the rats received normal saline and encountered to laparotomy, Sili: silibinin (60 mg/kg) was administered to animals, IR: the rats received the normal saline and insulted by liver IR procedure, and IR + Sili: silibinin was injected to rats. All groups were subjected to the same process of injection of the solvent or silibinin (30 min before laparotomy or ischemia and immediately after the reperfusion), intraperitoneally (IP). After 3 h of reperfusion, blood and liver tissue samples were collected for future examinations. Our results showed no significant differences between the Vehicle and Sili groups in all assessed parameters. In IR + Sili, the increased serum levels of AST and ALT in comparison with the control group were markedly reduced by silibinin treatment. Silibinin lowered the elevated expression of OPA1 and MFN1 mRNAs in the IR group. Histology revealed silibinin could decline tissue degeneration compared to the IR group. Electron microscopy of control and silibinin groups showed no fusion of mitochondria and tissue degradation both of which were observed in the IR group. The extent of tissue destruction and mitochondrial fusion decreased significantly with silibinin treatment. Silibinin has a protective effect on liver cells against IR induced injuries by preserving mitochondrial membrane.