mir-221, mir-190b, mir-363-3p, mir-200c are involved in rat liver ischaemia-reperfusion injury through oxidative stress, apoptosis and endoplasmic reticulum stress

Aim In this study, it was aimed to investigate the relationship between expression levels of micro-RNAs, endoplasmic reticulum (ER) stress, apoptosis and oxidative stress markers in hepatic ischaemia-reperfusion (IR) injury. Methods Sixteen rats were randomised into two groups: Sham and IR groups. In the IR group, portal vein and hepatic artery were totally clamped with an atraumatic microvascular clamp and 60 minutes later unclamped and finally IR model was accomplished (60 minutes ischaemia and 60 minutes reperfusion). After sacrification, serum insulin-like growth factor-1 (IGF-1), tumour necrosis factor-alpha (TNF-alpha), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver tissue samples were evaluated histopathologically. The expression levels of IR1-alpha, Perk, Catalase, Gpx-1, Caspase-3, Bcl-2 genes and miR-33a, miR-221, miR-190b, miR-363-3p, miR-200c, miR-223, miR-133b were measured by quantitative real-time polymerase chain reaction method. Results Biochemical parameters of the IR group showed significantly higher changes compared with the Sham group (P < .01). Histological tissue damage was significantly prominent in the IR group. ER stress, oxidative stress and apoptosis gene expression levels were significantly higher in the IR group (P < .01). Expression levels of miR-221, miR-190b, miR-363-3p and miR-200c were increased in the IR group compared with the Sham group. No significant difference was found between the two groups in terms of miR-33a, miR-133b and miR-223 expression levels (P > .05). Conclusion There is a strong need to enlighten the physiopathological and molecular mechanisms of liver IR injury and to find more specific biomarkers for IR damage, and miR-221, miR-190b, miR-363-3p and miR-200c maybe used as potential biomarkers of hepatic IR injury.