Transplantation proceedings · 2026
Mitochondrial Transplantation-Mediated Restoration of Mitochondrial Function Alleviates Hepatic Ischemia-Reperfusion Injury in Mice.
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Hua Yanling, Wang Zhiyu, Wang Minhao, Li Yiqun, Li Li
Аннотация
BACKGROUND: Hepatic ischemia-reperfusion injury (HIRI) is a major complication in liver surgery and transplantation, with mitochondrial dysfunction playing a central role. Mitochondrial transplantation has shown promise in other organ systems, but its effects and mechanisms in HIRI remain incompletely understood.
OBJECTIVE: This study aimed to investigate the protective effects of mitochondrial transplantation on HIRI and explore the underlying molecular mechanisms.
METHODS: HIRI was induced in male C57BL/6 mice by 60 minutes of partial hepatic ischemia followed by 3 hours of reperfusion. Autologous liver mitochondria (0.5 mg/kg) or vehicle were administered intravenously at the onset of reperfusion. In parallel, human THLE-2 hepatocytes were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) with or without mitochondrial supplementation (50 μg/mL). Liver injury (serum ALT/AST, measured as mass concentrations by ELISA), histopathology, cytokine profiles (TNF-α, IL-6, IL-10), apoptosis (Bax, Bcl-2, Cleaved Caspase-3, Annexin V), mitochondrial function (membrane potential, ROS production), and cell viability were assessed.
RESULTS: Mitochondrial transplantation was associated with significantly reduced serum ALT and AST levels and attenuated histopathological liver damage in vivo (**p < .01). These changes correlated with a shift in cytokine balance, characterized by lower TNF-α and IL-6 and higher IL-10 levels, and with reduced expression of pro-apoptotic markers. In vitro, mitochondrial supplementation was associated with improved hepatocyte viability, reduced enzyme leakage, modulated cytokine secretion, and decreased apoptosis following OGD/R. These protective effects correlated with preserved mitochondrial membrane potential and reduced mitochondrial superoxide production.
CONCLUSIONS: Our findings suggest that mitochondrial transplantation is associated with mitigation of HIRI in a murine model and with improved mitochondrial parameters in stressed hepatocytes. These correlative data support the potential of this approach as a therapeutic strategy for HIRI.
OBJECTIVE: This study aimed to investigate the protective effects of mitochondrial transplantation on HIRI and explore the underlying molecular mechanisms.
METHODS: HIRI was induced in male C57BL/6 mice by 60 minutes of partial hepatic ischemia followed by 3 hours of reperfusion. Autologous liver mitochondria (0.5 mg/kg) or vehicle were administered intravenously at the onset of reperfusion. In parallel, human THLE-2 hepatocytes were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) with or without mitochondrial supplementation (50 μg/mL). Liver injury (serum ALT/AST, measured as mass concentrations by ELISA), histopathology, cytokine profiles (TNF-α, IL-6, IL-10), apoptosis (Bax, Bcl-2, Cleaved Caspase-3, Annexin V), mitochondrial function (membrane potential, ROS production), and cell viability were assessed.
RESULTS: Mitochondrial transplantation was associated with significantly reduced serum ALT and AST levels and attenuated histopathological liver damage in vivo (**p < .01). These changes correlated with a shift in cytokine balance, characterized by lower TNF-α and IL-6 and higher IL-10 levels, and with reduced expression of pro-apoptotic markers. In vitro, mitochondrial supplementation was associated with improved hepatocyte viability, reduced enzyme leakage, modulated cytokine secretion, and decreased apoptosis following OGD/R. These protective effects correlated with preserved mitochondrial membrane potential and reduced mitochondrial superoxide production.
CONCLUSIONS: Our findings suggest that mitochondrial transplantation is associated with mitigation of HIRI in a murine model and with improved mitochondrial parameters in stressed hepatocytes. These correlative data support the potential of this approach as a therapeutic strategy for HIRI.