[Inhibition of lipopolysaccharide-induced inflammation in RAW264.7 macrophages by sinomenine through regulating heme oxygenase-1 expression and autophagy].

青藤碱 血红素加氧酶 脂多糖 化学 自噬 肿瘤坏死因子α 炎症 血红素 信使核糖核酸 免疫印迹 分子生物学 药理学 生物化学 免疫学 生物 细胞凋亡 基因
作者
Yue Peng,Hao Ou,Mingshi Yang,Yu Jiang,Min Gao
出处
期刊:PubMed 卷期号:43 (9): 964-970 被引量:1
标识
DOI:10.11817/j.issn.1672-7347.2018.09.006
摘要

OBJECTIVE: To investigate the effect of sinomenine on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 macrophages and the underlying mechanisms. Methods: The mouse RAW264.7 macrophages were treated with sinomenine and/or LPS with or without heme oxygenase-1 (HO-1) inhibitor Znpp. Real-time PCR, ELISA, immunofluenscence, and Western blot were used to detect the mRNA expression of TNF-α and IL-6, the release of TNF-α and IL-6, the protein expression of HO-1 and autophagy, respectively. Results: Compared with the control group, the mRNA expression and release of inflammatory cytokines TNF-α and IL-6 were increased, the green fluorescence of autophagy-related protein LC3 was accumulated and the protein expression of HO-1 was increased in RAW264.7 cells after LPS treatment (P<0.05). Compared with the LPS group, sinomenine treatment could reduce the mRNA expression and release of TNF-α and IL-6, accompanied by increasess in green fluorescence aggregation of LC3 and HO-1 production (P<0.05). HO-1 inhibitor Znpp could weaken the ability of sinomenine through suppressing TNF-α and IL-6 expression and decreasing the aggregation of LC3 green fluorescence (P<0.05). Conclusion: Sinomenine could alleviate LPS-induced inflammation in RAW264.7 macrophages, which might be related to HO-1 mediated autophagy. This study provides an experimental and theoretical basis for the clinical application of sinomenine in prevention and treatment of inflammation.
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