Evaluation of the effect of a single dose of morroniside on rat liver subjected to ischemia and reperfusion.

Introduction: Hepatic ischemia-reperfusion (IR) injury remains a major clinical problem during liver surgery and transplantation, primarily due to oxidative stress, inflammatory activation, and hepatocellular damage. Morroniside (MO), an iridoid glycoside derived from Methods: Wistar rats were divided into four groups: control (C), ischemia-reperfusion without treatment (CIR), and IR treated with MO at 90 mg/kg (90MIR) or 270 mg/kg (270MIR). Hepatic injury was assessed biochemically (ALT, AST, PIIINP, antioxidant capacity, cytokine profile), histologically and immunohistochemically (Collagen III, Survivin, HIF-1α, Caspase-8, IL-6). Results: IR induced significant hepatocellular injury, reflected by elevated aminotransferases, structural disruption, and increased pro-inflammatory cytokines. MO administration produced dose-dependent and heterogeneous effects. At 90 mg/kg, MO partially attenuated early aminotransferase elevation and reduced TNF-α and VEGF levels, suggesting initial hepatoprotective activity; however, hepatocellular damage and fibrosis markers remained elevated after 24 h. At 270 mg/kg, MO paradoxically decreased antioxidant capacity and did not suppress fibrosis or apoptosis, while only modestly reducing pro-inflammatory cytokines. Histopathological analyses confirmed pronounced liver injury in all IR groups regardless of treatment. Discussion: In conclusion, acute pre-procedural administration of MO did not provide consistent protection against hepatic IR injury, and its effects were dose-dependent and ambiguous. Further studies with prolonged dosing regimens and extended reperfusion times are warranted to clarify MO's hepatoprotective potential.