The present study aims to investigate the effects of Xuesaitong (XST)injection on inflammation induced by OGD/reoxygenation in BV2 microglia cell and explore the underlying mechanisms.The effects of XST injection were evaluated in terms of cell viability, secretion of TNF-α, IL-1β, IL-6 and IL-10 into culture media, protein expression of p-ERK1/2, p-JNK and p-p38, and nuclear translocation of NF-κB p65. The results showed that XST injection significantly increased cell viability, suppressed release of TNF-α, IL-1β, IL-6 and IL-10 and down-regulated p-JNK1/2 and p-p38 MAPK expression in BV2 microglia cells induced by OGD/R injury, whereas it had no effect on p-ERK1/2 expression. Furthermore, XST injection suppressed nuclear translocation of NF-κB p65 in BV2 microglia after OGD/R injury. These data indicate that the neuroprotective effects of XST injection on OGD/R injury are associated with its inhibition of pro-inflammatory mediator production, down-regulation of JNK1/2 and p38 MAPK activation, and suppression of NF-κB p65 nuclear translocation in BV2 microglia cells.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.19540/j.cnki.cjcmm.20161222.029 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Esketamine at a Clinical Dose Attenuates Cerebral Ischemia/Reperfusion Injury by Inhibiting AKT Signaling Pathway to Facilitate Microglia M2 Polarization and Autophagy.
Drug Des Devel Ther
January 2025
Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.
Purpose: This study aimed to assess the protective effect of a clinical dose esketamine on cerebral ischemia/reperfusion (I/R) injury and to reveal the potential mechanisms associated with microglial polarization and autophagy.
Methods: Experimental cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in adult rats and simulated by oxygen-glucose deprivation (OGD) in BV-2 microglial cells. Neurological and sensorimotor function, cerebral infarct volume, histopathological changes, mitochondrial morphological changes, and apoptosis of ischemic brain tissues were assessed in the presence or absence of esketamine and the autophagy inducer rapamycin.
Investigation of Novel Aronia Bioactive Fraction-Alginic Acid Nanocomplex on the Enhanced Modulation of Neuroinflammation and Inhibition of Aβ Aggregation.
Pharmaceutics
December 2024
Department of Pharmacy, College of Pharmacy, Ajou University, Suwon 16499, Republic of Korea.
Background/objectives: Aronia extract or its active compounds, especially anthocyanin, have shown potential for Alzheimer's disease (AD)-related pathologies, including neuroinflammation, fibrillogenesis of amyloid beta (Aβ), and cognitive impairment. However, there was still concern about their structural instability in vivo and in vitro. To solve the instability of anthocyanins, we combined aronia bioactive factions (ABFs) and alginic acid via electrostatic molecular interactions and created an ABF-alginic acid nanocomplex (AANCP).
View Article and Find Full Text PDFAnti-Neuroinflammatory Effects of Prenylated Indole Alkaloids from the Antarctic Fungus sp. Strain SF-7367.
Molecules
January 2025
Institute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, Iksan 54538, Republic of Korea.
Inflammation has always been considered a trigger or consequence of neurodegenerative diseases, and the inhibition of inflammation in the central nervous system can effectively protect nerve cells. Several studies have indicated that various natural products inhibit neuroinflammation. Among these, Antarctic fungal metabolites have pharmacological activities and a developmental value.
View Article and Find Full Text PDFA Network Pharmacology Study and Experimental Validation to Identify the Potential Mechanism of Heparan Sulfate on Alzheimer's Disease-Related Neuroinflammation.
Biomedicines
January 2025
Department of Pharmacology, School of Korean Medicine, Wonkwang University, Iksan 54538, Republic of Korea.
Background/objectives: Heparan sulfate (HS) is a polysaccharide that is found on the surface of cells and has various biological functions in the body.
Methods: The purpose of this study was to predict the pharmacological effects and molecular mechanisms of HS on Alzheimer's disease (AD) and neuroinflammation (NI) through a network pharmacology analysis and to experimentally verify them.
Results: We performed functional enrichment analysis of common genes between HS target genes and AD-NI gene sets and obtained items such as the "Cytokine-Mediated Signaling Pathway", "Positive Regulation Of MAPK Cascade", and "MAPK signaling pathway".
Stem-leaf saponins of Panax notoginseng attenuate experimental Parkinson's disease progression in mice by inhibiting microglia-mediated neuroinflammation via P2Y2R/PI3K/AKT/NFκB signaling pathway.
Chin J Nat Med
January 2025
Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, Institute of Chinese Materia Medica, The MOE Innovation Centre for Basic Medicine Research on Qi-Blood TCM Theories, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. Electronic address:
Stem-leaf saponins from Panax notoginseng (SLSP) comprise numerous PPD-type saponins with diverse pharmacological properties; however, their role in Parkinson's disease (PD), characterized by microglia-mediated neuroinflammation, remains unclear. This study evaluated the effects of SLSP on suppressing microglia-driven neuroinflammation in experimental PD models, including the 1-methyl-4-phenylpyridinium (MPTP)-induced mouse model and lipopolysaccharide (LPS)-stimulated BV-2 microglia. Our findings revealed that SLSP mitigated behavioral impairments and excessive microglial activation in models of PD, including MPTP-treated mice.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!