Anti-neuroinflammatory effects of alkaloid-enriched extract from Huperzia serrata on lipopolysaccharide-stimulated BV-2 microglial cellsopen access
- Authors
- Dang, Thu Kim; Hong, Seong-Min; Dao, Vui Thi; Tran, Phuong Thi Thu; Tran, Hiep Tuan; Do, Giang Hoang; Hai, Thanh Nguyen; Pham, Hang Thi Nguyet; Kim, Sun Yeou
- Issue Date
- Dec-2023
- Publisher
- TAYLOR & FRANCIS LTD
- Keywords
- Huperzine A; neurodegenerative diseases
- Citation
- PHARMACEUTICAL BIOLOGY, v.61, no.1, pp.135 - 143
- Journal Title
- PHARMACEUTICAL BIOLOGY
- Volume
- 61
- Number
- 1
- Start Page
- 135
- End Page
- 143
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/86758
- DOI
- 10.1080/13880209.2022.2159450
- ISSN
- 1388-0209
- Abstract
- Context Alkaloid-enriched extract of Huperzia serrata (Thunb.) Trevis (Lycopodiaceae) (HsAE) can potentially be used to manage neuronal disorders. Objective This study determines the anti-neuroinflammatory effects of HsAE on lipopolysaccharide (LPS)-stimulated BV-2 microglial cells and the underlying mechanisms. Materials and methods BV-2 cells were pre- or post-treated with different concentrations of HsAE (25-150 mu g/mL) for 30 min before or after LPS induction. Cell viability was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and no cytotoxicity was found. Nitric oxide (NO) concentration was determined using Griess reagent. The levels of prostaglandin E2 (PGE2), tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6 were determined using enzyme-linked immunosorbent assay. The levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 and the phosphorylation of mitogen-activated protein kinase (MAPK) were analyzed using western blotting. Results HsAE reduced LPS-induced NO production with half-maximal inhibitory concentration values of 99.79 and 92.40 mu g/mL at pre- and post-treatment, respectively. Pre-treatment with HsAE at concentrations of 50, 100, and 150 mu g/mL completely inhibited the secretion of PGE2, TNF-alpha, IL-6, and IL-1 beta compared to post-treatment with HsAE. This suggests that prophylactic treatment is better than post-inflammation treatment. HsAE decreased the expression levels of iNOS and COX-2 and attenuated the secretion of pro-inflammatory factors by downregulating the phosphorylation of p38 and extracellular signal-regulated protein kinase in the MAPK signaling pathway. Discussion and Conclusions HsAE exerts anti-neuroinflammatory effects on LPS-stimulated BV-2 cells, suggesting that it may be a potential candidate for the treatment of neuroinflammation in neurodegenerative diseases.
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