Inhibition of telomerase activity by BIBP1532 abolished the protective role of irisin in increasing autophagy and mitochondrial function during hepatic H/R. Old rat hepatocytes were isolated, and the hypoxia reoxygenation (H/R) model was performed in hepatocytes by exposing to hypoxia condition (94% N₂, 5% CO₂, and 1% O₂) at 37°C in glucose/FBS-free RPMI-1640 medium. One hour later, the hepatocytes returned to normal culture conditions. The sham group was treated with normal medium without hypoxia. BIBR 1532 was administrated at the beginning of reoxygenation (50 μM). The subsequent experiments were performed at 8 h after reoxygenation. (a–c) Western blot analysis of liver irisin and TERT expression. (d–f) Western blot analysis of liver LC3B and P62 expression. (g–i) Western blot analysis of liver PGC1α and TFAM expression. Partial (70%) liver arterial/portal venous blood was interrupted for 40 minutes in 3-month- and 22-month-old rats. Blood samples were harvested at 24 h after reperfusion. Partial (70%) liver arterial/portal venous blood was interrupted for 40 minutes in 3-month-old rats. Irisin (iv. 250 μg/kg, single dose) and BIBR 1532 (iv. 20 mg/kg, single dose) were administrated in young rats at the beginning of reperfusion. (j) TUNEL (green) and H&E staining of the liver. (k) Percentage of TUNEL-positive cells. (l) Percentage of necrotic areas. (m) Liver histological scores. (n) Serum ALT. ; ; and .