Polyphenols from Securidaca inappendiculata alleviated acute lung injury in rats by inhibiting oxidative stress sensitive pathways

• 作者: Cong-lan Ji Sheng Dai Hong Liu Ji-yang Dong Chun-sheng Liu Jian Zuo
• 来源期刊: 中草药（英文版）
• 年，卷（期）: 2021,（3）
• 所属期刊栏目: Original Articles
• 页码范围: 381-388
• 页数: 8页
• 语种: 英文

摘要

Objective:Securidaca inappendiculata is a medicinal plant frequently used in the treatment of inflamma-tory diseases in south China.In this study,we aimed to explore its bioactive constituent which con-tributes to the anti-inflammatory activity.Methods:Polyphenol-enriched and polyphenol-deprived fractions(PRF and PDF,respectively)were sep-arated from the ethanolic extract by HPD300 macroporous resin-based method,and their anti-inflammatory activities were investigated on a lipopolysaccharide(LPS)-induced acute lung injury(ALI)model in rats.The possible mechanism of action in alleviating acute inflammation was studied using RAW264.7 cells.Results:Both Folin-Ciocalteu and 1H nuclear magnetic resonance(NMR)analyses showed that polyphe-nolic content in PRF was approximately 10 times higher than that of PDF,and this observation reflected in their antioxidative capacities.PRF but not PDF significantly decreased the level of malondialdehyde,sup-pressed the expression of nicotinamide phosphoribosyltransferase(NAMPT)protein,and improved the severity of ALI in rats.PRF at 10 μg/mL effectively downregulated the expression of proteins NAMPT,HMGB1,TLR4,and p-p65,and scavenged the intracellular reactive oxygen species(ROS)in LPS-primed RAW264.7 cells.N-acetyl-L-cysteine exhibited similar inhibitory effects on ROS production and NAMPT-mediated TLR4/NF-κB activation in vitro,whereas nicotinamide mononucleotide antagonized all the changes induced by PRF during cotreatments.Conclusion:As an antioxidant,PRF exhibited potent anti-inflammatory activity under both in vivo and in vitro conditions by downregulating NAMPT and TLR4/NF-κB.Accordingly,polyphenols were identified as important bioactive constituents in S.inappendiculata targeting oxidative stress-sensitive pro-inflammatory pathways.