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

IF 2.3 4区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Membrane Biology Pub Date : 2025-02-12 DOI:10.1007/s00232-025-00340-9

Fei Hu, Songlin Tong, Hongming Xu

{"title":"Schisandrin B Improves Mitochondrial Function and Inhibits HT22 Cell Apoptosis by Regulating Sirt3 Protein.","authors":"Fei Hu, Songlin Tong, Hongming Xu","doi":"10.1007/s00232-025-00340-9","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":50129,"journal":{"name":"Journal of Membrane Biology","volume":" ","pages":""},"PeriodicalIF":2.3000,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Membrane Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s00232-025-00340-9","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

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.

查看原文本刊更多论文

求助全文

约1分钟内获得全文求助全文

来源期刊

Journal of Membrane Biology 生物-生化与分子生物学

CiteScore

4.80

自引率

4.20%

发文量

审稿时长

6-12 weeks

期刊介绍： The Journal of Membrane Biology is dedicated to publishing high-quality science related to membrane biology, biochemistry and biophysics. In particular, we welcome work that uses modern experimental or computational methods including but not limited to those with microscopy, diffraction, NMR, computer simulations, or biochemistry aimed at membrane associated or membrane embedded proteins or model membrane systems. These methods might be applied to study topics like membrane protein structure and function, membrane mediated or controlled signaling mechanisms, cell-cell communication via gap junctions, the behavior of proteins and lipids based on monolayer or bilayer systems, or genetic and regulatory mechanisms controlling membrane function. Research articles, short communications and reviews are all welcome. We also encourage authors to consider publishing ''negative'' results where experiments or simulations were well performed, but resulted in unusual or unexpected outcomes without obvious explanations. While we welcome connections to clinical studies, submissions that are primarily clinical in nature or that fail to make connections to the basic science issues of membrane structure, chemistry and function, are not appropriate for the journal. In a similar way, studies that are primarily descriptive and narratives of assays in a clinical or population study are best published in other journals. If you are not certain, it is entirely appropriate to write to us to inquire if your study is a good fit for the journal.