Exploring the mechanism of Wogonin in the attenuation of LPS-induced inflammation in BV-2 cells and the protective effect of wogonin on SH-SY5Y cells

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Abstract

Parkinson's disease (PD) is a neurodegenerative disease that affects mainly middle-aged and elderly people, and its pathogenesis has not been clarified. To model neuroinflammatory components of PD in vitro, lipopolysaccharide (LPS)-induced inflammatory injury in BV-2 microglial cells was employed. Wogonin is a natural bioflavonoid extracted from the rhizome of the Chinese herb Scutellaria baicalensis . It has a neuroprotective effect and can play a role in alleviating the symptoms of neurodegenerative diseases. The aim of this study was to investigate the mitigating effect of wogonin on lipopolysaccharide-induced inflammation in BV-2 cells and the protective effect on SH-SY5Y cells by an experimentally validated method. The CCK-8 assay was used to detect the cell viability of each group. Enzyme-linked immunosorbent assay (ELISA), immunohistochemical staining (IHC), immunofluorescence staining (IF) and Western blot methods (WB) were used to detect the cell pathway indicators and inflammatory factors in each group. The results showed that LPS (1 µg/mL) induced polarization and activation of BV-2 cells and significantly increased the release of pro-inflammatory factors IL-6, TNF-α, and IL-1β, while decreasing the expression of tyrosine hydroxylase (TH) and promoting the aberrant aggregation of α-synaptic nucleoprotein (α-Syn) in SH-SY5Y neurons. After intervention with wogonin (16 µM), the above pathological processes were effectively reversed: inhibition of inflammatory factor secretion in BV-2 cells, restoration of TH expression in SH-SY5Y neurons, reduction of α-Syn deposition, and reduction of NF-κB p65 nuclear translocation and activation of the TLR4/MyD88 pathway. The effect was comparable to that of a TLR4 inhibitor (TAK-242), but the combination of the two did not show a synergistic effect. The study suggests that wogonin may inhibit LPS-induced release of inflammatory factors from BV-2 microglia and protect SH-SY5Y cells by regulating the TLR4/MyD88/NF-κB signaling pathway.

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