ArticleThe Kaohsiung journal of medical sciences2022
Senkyunolide H inhibits activation of microglia and attenuates lipopolysaccharide-mediated neuroinflammation and oxidative stress in BV2 microglia cells via regulating ERK and NF-κB pathway.
Article in The Kaohsiung journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- A Coumarin- and Phthalide-Rich Fraction From Baichuan Baile Formula Alleviates Reserpine-Induced Depression-Like Behaviors by Modulating the Monoaminergic System and Gut Microbiota.Chemistry & biodiversity · 2026Article
- Senkyunolides: a promising natural compounds for the treatment of migraine headaches.Frontiers in nutrition · 2026Review
- Senkyunolide H reverses depression-induced breast cancer progression by regulating CXCR2.Natural products and bioprospecting · 2025Article
- Studying the efficacy of JBOL volatile components in idiopathic pulmonary fibrosis (IPF) using GC-MS and network pharmacology.Scientific reports · 2025Article
- Review
- Jiawei Kongsheng Zhenzhong Pill: marker compounds, absorption into the serum (rat), and Q-markers identified by UPLC-Q-TOF-MS/MS.Frontiers in pharmacology · 2024Article
- Effects ofInternational journal of molecular sciences · 2023Article
- Gap Junctions and Connexins in Microglia-Related Oxidative Stress and Neuroinflammation: Perspectives for Drug Discovery.Biomolecules · 2023Review
- Senkyunolide H inhibits activation of microglia and attenuates lipopolysaccharide-mediated neuroinflammation and oxidative stress in BV2 microglia cells via regulating ERK and NF-κB pathway.The Kaohsiung journal of medical sciences · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain is one of the common surgical diseases, which leads to abnormal chronic pain and pain hypersensitivity reaction. Microglia are important glial cells in the spinal cord, which are conducive to sensitization and maintenance of chronic pain. Recently, Senkyunolide H (SNH) has been reported to play an anti-inflammatory and antioxidant role. However, the mechanisms by which SNH improves neuropathic pain symptoms remain unknown. This study aimed to evaluate and identify the role of SNH in lipopolysaccharide (LPS)-mediated neuroinflammation and oxidative stress in BV2. Western blot and immunostaining assays revealed that SNH treatment attenuated LPS-mediated activation of BV2 in a dose-dependent manner. Flow cytometry further verified that BV2 microglial cells gradually shifted from an M1 (pro-inflammatory) phenotype to an M2 (anti-inflammatory) phenotype after SNH administration. Furthermore, quantitative real-time polymerase chain reaction and ELISA assays demonstrated that SNH treatment attenuated LPS-mediated neuroinflammation and oxidative stress in BV2 microglial cells. Lastly, western blot assays suggested that SHN could inactivate the ERK and NF-κB signaling pathways. Altogether, our findings have demonstrated that SNH could reverse LPS-mediated activation of microglia, LPS-mediated neuroinflammation and oxidative stress in BV2 via regulating the ERK and NF-κB pathways.
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