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ORIGINAL ARTICLE
Year : 2020  |  Volume : 16  |  Issue : 71  |  Page : 675-680

Glabridin downregulates lipopolysaccharide-induced oxidative stress and neuroinflammation in BV-2 microglial cells via suppression of nuclear factor-κB signaling pathway


Department of Neurology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China

Correspondence Address:
Lianmei Zhong
Department of Neurology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_497_19

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Background: Microglia initially undergoes chronic activation in response to the damages caused by stressful stimuli, such as bacterial infection and hypoxia. Inflammatory responses, as well as oxidative stress, perform crucial roles in the process of neuroinflammation, which results in brain damage. Glabridin is a natural organic compound with extensive beneficial properties such as anti-inflammatory and antioxidant properties. To the best of our knowledge, there are no studies conducted on the anti-neuroinflammatory activity of glabridin. Therefore, in this study, we aimed to investigate the potency of glabridin against the expression of lipopolysaccharide (LPS)-stimulated BV-2 cells. Materials and Methods: BV-2 cells were preincubated with glabridin followed by the LPS challenge. Subsequently, the cellular status of nitric oxide (NO), reactive oxygen species (ROS), prostaglandin E2(PGE2), and pro-inflammatory modulators (interleukin [IL]-1β and IL-6) were investigated and related signaling pathways were inspected via blotting assay. Results: Our results indicate that glabridin appreciably alleviated the LPS-induced accretion of inducible-NO synthase (iNOS), PGE2, IL-1β, and IL-6. Moreover, it noticeably allayed the NO/iNOS, PGE2/cyclooxygenase-2 protein statuses, and pro-inflammatory cytokine (tumor necrosis factor-α) on LPS-induced microglia. We also found that LPS severely increased the phosphorylation of Inhibitory kappa B kinases (IKKs), IκBα, p65, and nuclear factor (NF)-κB. Although glabridin supplementation suppressed the phosphorylation of the aforementioned molecules, LPS remarkable caused the nuclear interchange of NF-κBp65. Conclusion: Glabridin alleviates LPS-induced neuroinflammation in BV-2 cells by suppressing the accumulation of ROS and cell death and by inhibiting the pro-inflammatory responses via NF-κB-dependent mechanisms. According to our results, glabridin may be beneficial in neuroinflammation-related neurodegenerative disorders.


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