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Silibinin treatment results in reducing OPA1&MFN1 genes expression in a rat model hepatic ischemia-reperfusion.
Molecular Biology Reports ( IF 2.6 ) Pub Date : 2020-04-05 , DOI: 10.1007/s11033-020-05383-w
Neda Masoumi Qajari 1 , Majid Malekzadeh Shafaroudi 2, 3 , Milad Gholami 4 , Abbas Khonakdar-Tarsi 1, 3, 5, 6
Affiliation  

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.

中文翻译:

水飞蓟宾治疗可降低大鼠肝缺血再灌注模型中OPA1和MFN1基因的表达。

线粒体损伤在触发细胞凋亡和细胞死亡中起关键作用。这项研究评估了水飞蓟宾对肝温暖缺血再灌注(IR)期间肝脏组织中光学萎缩-1(OPA1)和mitofusin-1(MFN1)基因表达的影响。将大鼠分为四组,每组八只:媒介物:大鼠接受生理盐水剖腹手术;思利:水飞蓟宾(60 mg / kg)施用于动物; IR:大鼠接受生理盐水并受到肝脏IR损伤程序,IR + Sili:水飞蓟宾注射到大鼠。所有组均经腹膜内(IP)进行相同的溶剂或水飞蓟宾注射步骤(剖腹术或局部缺血前30分钟,再灌注后立即注射)。再灌注3小时后,收集血液和肝组织样本以备将来检查。我们的结果表明,在所有评估参数中,车辆和Sili组之间没有显着差异。在IR + Sili中,水飞蓟宾治疗显着降低了血清AST和ALT与对照组相比的升高。水飞蓟宾降低IR组中OPA1和MFN1 mRNA的表达升高。组织学显示,与IR组相比,水飞蓟宾可降低组织变性。对照组和水飞蓟宾组的电子显微镜观察未见线粒体融合和组织降解,IR组均观察到。水飞蓟宾治疗可显着降低组织破坏和线粒体融合的程度。水飞蓟宾通过保存线粒体膜对肝细胞具有保护作用,使其免受IR诱导的损伤。
更新日期:2020-04-06
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