Physcion prevents induction of optic nerve injury in rats via inhibition of the JAK2/STAT3 pathway.

Optic nerve injury is a type of neurodegenerative disease. Physcion is an anthraquinone that exerts a protective role against various diseases. However, its function in regulating optic nerve injury remains largely unknown. An model of optic nerve injury was established in HAPI cells treated with IFN-β. Functional assays were used to detect HAPI cell viability and apoptosis. The levels of inflammation and the expression levels of oxidative stress-related genes were measured in HAPI cells. In addition, western blot analysis was used to detect the expression levels of Janus kinase 2 (JAK2)/STAT3-linked genes in HAPI cells. Treatment of the cells with physcion prevented cells against IFN-β-induced neuronal injury. Physcion restrained IFN-β-induced inflammatory response and oxidative stress in HAPI cells. In addition, it improved IFN-β-induced injury in HAPI cells by suppressing the JAK2/STAT3 pathway. In conclusion, the present study revealed that physcion improved optic nerve injury by inhibiting the JAK2/STAT3 pathway. Physcion may be a promising therapeutic target for the treatment of this disease.