Schisandrin B Improves Mitochondrial Function and Inhibits HT22 Cell Apoptosis by Regulating Sirt3 Protein

Neurological diseases refer to pathological changes that occur in the brain, spinal cord, and peripheral nerves. Their etiologies are complex, treatment outcomes are poor, and prognoses are unfavorable. Therefore, how to improve the treatment efficacy of neurological diseases is an urgent problem to be addressed in current clinical practice. Schisandrin B, a commonly used traditional Chinese medicine in clinical settings, has anti-tumor, anti-inflammatory, and wound-healing promoting effects. However, there are relatively few studies on its application in the treatment of neurological diseases. In this study, HT22 nerve cells were cultured, and an injury model was constructed by applying H₂O₂ stimulation to explore the protective effect of Schisandrin B on these cells. The research results showed that compared with the H₂O₂ group, Schisandrin B could significantly increase the viability (30.872%) and migration ability (42.756%) of HT22 cells, and inhibit the apoptosis of HT22 cells (22.817%). Further exploration of the mechanism revealed that Schisandrin B regulated the mitochondrial dynamic balance and membrane potential level of HT22 cells by upregulating the expression of Sirt3 protein, enhanced the mitochondrial energy metabolism (with an increase of 53.411% in ATP production), and maintained the integrity of the quantity and structure of mitochondria, ultimately exerting a protective effect on HT22 cells.