Abstract
Liver ischemia/reperfusion injury (LIRI) is a common complication of liver surgery, and affects liver function post‑transplantation. However, the precise mechanism underlying LIRI has not yet been completely elucidated. Previous studies have demonstrated the involvement of a number of microRNAs (miRNAs/miRs) in liver pathophysiology. The objective of the present study was to determine the potential function and mechanism of miR‑101‑mediated regulation of autophagy in LIRI. Compared with the sham‑treated group, a significant decrease in miR‑101 and mechanistic target of rapamycin (mTOR) expression levels following ischemia/reperfusion (IR) were observed, along with an increased number of autophagosomes (P<0.001). The exogenous overexpression of miR‑101 has been demonstrated to inhibit autophagy during the LIRI response and the levels of mTOR and phosphorylated (p)‑mTOR expression are correspondingly elevated. However, compared with the miR‑NC group, miR‑101 silencing was associated with reduced mTOR and p‑mTOR levels and increased autophagy, as indicated by the gradual increase in the levels of the microtubule‑associated protein 1 light II (LC3II). The peak levels of LC3II were observed 12 h subsequent to reperfusion, which coincided with the lowest levels of miR‑101. In addition, inhibition of autophagy by 3‑methyladenine significant enhanced the protective effect of miR‑101 against LIRI, compared with the IR group (P<0.001). Altogether, miR‑101 attenuates LIRI by inhibiting autophagy via activating the mTOR pathway.