4.7 Article

Chinese Medicine Formula Kai-Xin-San Ameliorates Neuronal Inflammation of CUMS-Induced Depression-like Mice and Reduces the Expressions of Inflammatory Factors via Inhibiting TLR4/IKK/NF-κB Pathways on BV2 Cells

Journal

FRONTIERS IN PHARMACOLOGY
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2021.626949

Keywords

Kai-Xin-San; neuronal inflammation; toll like receptor 4; NF-κ B; Chinese medicine formulae

Funding

  1. National Natural Science Foundation of China [81673720, 81973591]
  2. Open Project Program of Jiangsu Key Laboratory for High Technology Research of TCM Formulae and Jiangsu Collaborative Innovation Centre of Chinese Medicinal Resources Industrialization [FJGJS-201510]
  3. fifth phase of the 333 high-level personnel training project of Jiangsu Province [BRA2017463]
  4. Innovation projects of scientific research for the graduate student in Jiangsu province [KYCX20_1598]
  5. 2020 Jiangsu University Students Innovation and Entrepreneurship Training Program Project [202010315043Y]
  6. Jiangsu province official health research project [BJ19009]
  7. Suzhou people's livelihood Science and Technology demonstration Project [SS202006]

Ask authors/readers for more resources

Research suggests that Kai-Xin-San may exert its antidepressant effects by regulating pro-inflammatory cytokines in microglia, providing scientific evidence for its development as an alternative therapy for major depressive disorder.
Kai-Xin-San (KXS) is a traditional Chinese medicinal formula composed of Ginseng Radix et Rhizoma, Polygalae Radix, Acori Tatarinowii Rhizoma, and Poria for relieving major depressive disorder and Alzheimer's disease in traditional Chinese medicine (TCM) clinics. Previous studies on the antidepressant mechanism of KXS mainly focused on neurotransmitter and neurotrophic factor regulation, but few reports exist on neuronal inflammation regulation. In the current study, we found that KXS exerted antidepressant effects in chronic unpredictable mild stress-induced depression-like mice according to the results of behavioral tests. Meanwhile, KXS also inhibited the activation of microglia and significantly reduced the expression of pro-inflammatory cytokines such as IL-1 beta, IL-2, and TNF-alpha in the hippocampus of mice. In mice BV2 microglia cell lines, KXS extract reduced the expression of inflammatory factors in BV2 cells induced by lipopolysaccharide via inhibiting TLR4/IKK/NF-kappa B pathways, which was also validated by the treatment of signaling pathway inhibitors such as TAK-242 and JSH-23. T0hese data implied that the regulation of pro-inflammatory cytokines in microglia might account for the antidepressant effect of KXS, thereby providing more scientific information for the development of KXS as an alternative therapy for major depressive disorder.

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