Oxidative stress and mitochondrial dysfunction play a crucial role in the progression of hepatic encephalopathy, however, specific and effective therapeutic options remain limited, and the precise molecular mechanisms and direct targets by which Silibinin meglumine ameliorates HE remain incompletely elucidated.
Here, we elucidate the hepatoprotective and neuroprotective effects of SM in a thioacetamide (TAA)-induced HE mouse model and in vitro hepatocytes, and demonstrate that it improves liver function and reduces neuroinflammation by directly binding to and downregulating UCP2 expression. SM alleviates oxidative stress and mitochondrial dysfunction through modulation of the UCP2/PINK1/Drp1/MFN2/LC3B pathway, thereby suppressing excessive mitophagy and restoring mitochondrial homeostasis.
This work provides a comprehensive theoretical foundation identifying UCP2 as a direct target of SM and clarifies the critical role of UCP2-mediated mitophagy regulation in HE progression. The work entitled “ Silibinin meglumine ameliorates hepatic encephalopathy via inhibiting UCP2-mediated oxidative stress and mitochondrial dysfunction ” was published on Chinese Journal of Natural Medicines (published on May 20, 2026).
Chinese Journal of Natural Medicines
Experimental study
Not applicable
Silibinin meglumine ameliorates hepatic encephalopathy via inhibiting UCP2-mediated oxidative stress and mitochondrial dysfunction
20-May-2026