Anti-inflammatory Mechanism of Action of Benzoylmesaconine in Lipopolysaccharide-Stimulated RAW264.7 Cells. (13th July 2022)

• Record Type: Journal Article
• Authors: Zhou, Changkai; Gao, Jing; Qu, Haijun; Xu, Long; Zhang, Bin; Guo, Qie; Jing, Fanbo
• Other Names: Hu Weicheng Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2022(2022)
• Publication Date: 2022-07-13
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2022/7008907
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Background. Benzoylmesaconine (BMA), the most abundant monoester alkaloid in Aconitum plants, has some biological activities and is a potential therapeutic agent for inflammation-related diseases. However, the potential anti-inflammatory mechanisms of BMA have not been clarified. Purpose. This study aimed to investigate the underlying molecular mechanisms of the anti-inflammatory action of this compound using lipopolysaccharide (LPS)-activated RAW264.7 macrophages. Methods. The release of pro-inflammatory cytokines and mediators were detected by nitric oxide (NO) assays, reactive oxygen species (ROS) assays, and enzyme-linked immunosorbent assays (ELISA) in LPS-activated RAW264.7 macrophage cells. Quantitative real-time PCR was used to measure the gene expression of interleukin (IL)-1 β, tumor necrosis factor (TNF)- α, IL-6, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Cell viability was determined using a cell counting kit-8 (CCK-8) assay. The expression of iNOS, COX-2, mitogen-activated protein kinase (MAPK), and nuclear factor- κ B (NF- κ B)-related proteins were detected by western blot, and nuclear translocation of p65 was observed by immunofluorescence. Results. BMA significantly decreased the production of IL-1 β, IL-6, TNF- α, PGE2, NO, and ROS and inhibited the protein and mRNA levels of COX-2 and iNOS in LPS-activated RAW264.7 macrophages. Moreover, LPS-induced phosphorylation of I κ B α, JNK, p38, and ERK; degradation of I κ B α ; and nuclear translocation of p65 were significantly suppressed by BMA treatment. Conclusion. These findings demonstrate that the anti-inflammatory effect of BMA was through the suppression of the NF- κ B and MAPK signaling pathways and that it may be a therapeutic agent targeting specific signal transduction events required for inflammation-related diseases.