The Role of Panax Notoginseng Saponins on Neuronal Oxidative Stress and Autophagy Response in Craniocerebral Injury Model Rats

Abstract

This study assessed how IL-6 affects the body’s autophagy status by regulating JAK-STAT3 and explored the mechanism by which IL-6 inhibits JAK-STAT3 signaling pathway-mediated autophagy, and how Panax notoginseng total saponins promote neuronal cell regeneration in rats. A model of neuronal oxidative stress in craniocerebral injury model rats was established, and IL-6 levels were detected by ELISA. Rat neuronal cells were isolated and cultured, while dual-luciferase gene reporter experiments analyzed the targeting relationship between IL-6 and JAK. qRT-PCR detected expression of neuronal autophagy-related genes (JAK, STAT3, ULK1, OsATG7, FAM176A, and Beclin 1). The level of IL-6 in the craniocerebral injury model was significantly higher than that in the control group. IL-6 binds to 3′-UTR of JAK, and transfection with IL-6 inhibitor increases the relative luciferase activity. pMIR-JAK-mut group has no significant effect. There is a targeted regulatory relationship between IL-6 and JAK. Adding total saponins of Panax notoginseng combined with nursing intervention can promote reduction genetic expression related to neuronal autophagy damage. IL-6 can target and regulate JAK gene. IL-6 can promote neuronal development by regulating JAK-STAT3. Autophagy repairs damage and inhibits the autophagy state of cells. Panax notoginseng total saponins are effective medicinal components extracted from high quality panax notoginseng according to extraction and separation technology. The results from this study provide a better understanding of pathogenesis of neuronal oxidative stress in craniocerebral injury model rats and find potential intervention targets, which will provide more treatment methods for neuronal oxidative stress damage in craniocerebral injury model rats.