Effects of silibinin on hepatic warm ischemia-reperfusion injury in the rat model.
ET-1
KLF2
Liver Ischemia/reperfusion
Silibinin
eNOS
Journal
Iranian journal of basic medical sciences
ISSN: 2008-3866
Titre abrégé: Iran J Basic Med Sci
Pays: Iran
ID NLM: 101517966
Informations de publication
Date de publication:
Jul 2019
Jul 2019
Historique:
entrez:
7
5
2020
pubmed:
7
5
2020
medline:
7
5
2020
Statut:
ppublish
Résumé
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. 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 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. 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.
Identifiants
pubmed: 32373301
doi: 10.22038/ijbms.2019.34967.8313
pmc: PMC7196349
doi:
Types de publication
Journal Article
Langues
eng
Pagination
789-796Références
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