Polypeptides Isolated from Lactococcus lactis Alleviates Lipopolysaccharide (LPS)-Induced Inflammation in Ctenopharyngodon idella

文献类型： 外文期刊

第一作者： Li, Pei

作者： Li, Pei;Li, Pei;Xu, Youqing;Ding, Zhaokun;Li, Pei;Cao, Yupo

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关键词： polypeptide; Lactococcus lactis; Ctenopharyngodon idella; lipopolysaccharide; bioassay-guided isolation; anti-inflammatory

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：6.208； 五年影响因子：6.628 ）

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年卷期： 2022 年 23 卷 12 期

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收录情况： SCI

摘要： The main purpose of the present study was to evaluate the anti-inflammatory activity of Lactococcus lactis BL52 and isolate active substances responsible for anti-inflammatory activity. Head-kidney (HK) macrophages were used for in vitro bioassay-guided isolation, and the structure of the two peptides was identified by mass spectrometry analysis. Lipopolysaccharide (LPS)-induced inflammatory responses in Ctenopharyngodon idella were also examined to evaluate the in vivo anti-inflammatory activity of active substances. Two active peptides were isolated by HPLC from L. lactis BL52, and an in vitro anti-inflammatory assay demonstrated that peptide ALBL1 and ALBL2 dose-dependently inhibited LPS-induced inflammatory cytokines TNF-alpha, IL-6, and IL-1 beta and inflammatory factors NO and PGE 2 production in macrophages (p < 0.05). After being treated with 20 mg/Kg peptide ALBL1 and ALBL2, the expression levels of TNF-alpha, IL-6, IL-1 beta, NO, and PGE 2 were significantly inhibited (p < 0.05). Results from the in vivo test showed that when the concentration of peptide ALBL1 and ALBL2 reached 30 mg/Kg, the LPS-induced upregulations of TNF-alpha, IL-6, IL-1 beta, NO, and PGE 2 were prevented. In addition, peptide ALBL1 and ALBL2 blocked the expression of Toll-like receptor 2 (TLR2) and then suppressed the phosphorylation of nuclear transcription factor-kappa B (NF-kappa B) p65 and degradation inhibitor of I kappa B alpha. Moreover, C. idella treated with peptide ALBL1 and ALBL2 can relieve pathological inflammatory responses caused by LPS. These results suggest that the anti-inflammatory properties of peptide ALBL1 and ALBL2 might be a result from the inhibition of IL-6, IL-1 beta, and TNF-alpha expressions through the downregulation of Toll2/NF-kappa B signaling pathways.

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