Anti-neuroinflammatory effects of alkaloid-enriched extract from Huperzia serrata on lipopolysaccharide-stimulated BV-2 microglial cells

• Published in: Pharmaceutical biology Vol. 61; no. 1; pp. 135 - 143
• Main Authors: Dang, Thu Kim, Hong, Seong-Min, Dao, Vui Thi, Tran, Phuong Thi Thu, Tran, Hiep Tuan, Do, Giang Hoang, Hai, Thanh Nguyen, Nguyet Pham, Hang Thi, Kim, Sun Yeou
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01-12-2023; Taylor & Francis Ltd; Taylor & Francis Group
• Subjects: Alkaloids; Alkaloids - metabolism; Alkaloids - pharmacology; Cell viability; Cyclooxygenase-2; Cytotoxicity; Dinoprostone - metabolism; Enzyme-linked immunosorbent assay; Extracellular Signal-Regulated MAP Kinases - metabolism; Huperzia - metabolism; Huperzia serrata; Huperzine A; Inflammation; Interleukin 6; Interleukin-6 - metabolism; Kinases; Lipopolysaccharides; Lipopolysaccharides - pharmacology; MAP kinase; Microglia; Microglial cells; Neurodegenerative diseases; Neuroinflammatory Diseases; NF-kappa B - metabolism; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - metabolism; Nitric-oxide synthase; Phosphorylation; Prostaglandin E2; Protein kinase; Signal transduction; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Western blotting; Huperzine A; neurodegenerative diseases
• ISSN: 1388-0209; 1744-5116
• DOI: 10.1080/13880209.2022.2159450

Alkaloid-enriched extract of Huperzia serrata (Thunb.) Trevis (Lycopodiaceae) (HsAE) can potentially be used to manage neuronal disorders.
This study determines the anti-neuroinflammatory effects of HsAE on lipopolysaccharide (LPS)-stimulated BV-2 microglial cells and the underlying mechanisms.
BV-2 cells were pre- or post-treated with different concentrations of HsAE (25-150 µg/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)-α, interleukin (IL)-1β, 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.
HsAE reduced LPS-induced NO production with half-maximal inhibitory concentration values of 99.79 and 92.40 µg/mL at pre- and post-treatment, respectively. Pre-treatment with HsAE at concentrations of 50, 100, and 150 µg/mL completely inhibited the secretion of PGE2, TNF-α, IL-6, and IL-1β 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.
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.