Effects of silibinin on hepatic warm ischemia-reperfusion injury in the rat model
محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 22، شماره: 7
سال انتشار: 1398
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 400
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شناسه ملی سند علمی:
JR_IJBMS-22-7_012
تاریخ نمایه سازی: 20 مهر 1398
چکیده مقاله:
Objective(s): Liver ischemia-reperfusion injuries (I/RI) are typically the main causes of liver dysfunction after various types of liver surgery especially liver transplantation. Radical components are the major causes of such direct injuries. We aimed to determine the beneficial effects of silibinin, a potent radical scavenger on liver I/RI.Materials and Methods: Thirty-two rats were divided into 4 groups. Group I: VEHICLE, the rats underwent laparotomy and received DMSO, group II: SILI, laparotomy was done and silibinin was administered. Group III: I/R, the rats received DMSO and were subjected to a liver I/R procedure and group IV: I/R+SILI, the animals underwent the I/R procedure and received silibinin. After 1 hr of ischemia followed by 3 hr reperfusion, blood was collected to evaluate the serum marker of liver injuries. Hepatic tissue was harvested to investigate glycogen content, histological changes, and vasoregulatory gene expression.Results: Results showed that serum AST, ALT, LDH, GGT, ALP, and hyaluronic acid (HA) increased significantly in I/R group compared with the VEHICLE group. Silibinin reduced this elevation except for GGT. Silibinin inhibited hepatocyte vacuolization and degeneration, endothelium damages, sinusoidal congestion and inflammation, and glycogen depletion during I/R. ET-1 mRNA was overproduced in the I/R group compared with the VEHICLE group which was decreased by silibinin. KLF2 and eNOS expression was reduced during I/R compared with the VEHICLE group. Silibinin elevated KLF2 expression but had no meaningful effect on eNOS expression.Conclusion: Silibinin protected the liver from I/RI. Silibinin could improve liver circulation by preventing sinusoidal congestion, inflammation, and perhaps modification of the vasoregulatory gene expression.
کلیدواژه ها:
نویسندگان
Vahid Akbari-Kordkheyli
Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran
Soheil Azizi
Department of Laboratory Medicine, Faculty of Allied Medical Sciences, Mazandaran University of Medical Sciences, Sari, Iran
Abbas Khonakdar-Tarsi
Department of Biochemistry, Biophysics and Genetics, Cellular and molecular biology research center, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
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