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氢气促进坏死性小肠结肠炎巨噬细胞极化过程中的M1巨噬细胞转化。

Hydrogen Promotes the M1 Macrophage Conversion During the Polarization of Macrophages in Necrotizing Enterocolitis.

作者信息

Yu Shenghua, Lv ZhiBao, Gao Zhimei, Shi Jingyi, Sheng Qingfeng, Zheng Lulu, Zhou Junmei, Wang Xueli

机构信息

Department of Pediatric Surgery, Shanghai Children's Hospital, Shanghai, China.

Department of Center Laboratory, Shanghai Children's Hospital, Shanghai, China.

出版信息

Front Pediatr. 2021 Nov 17;9:710382. doi: 10.3389/fped.2021.710382. eCollection 2021.

Abstract

Hydrogen is protective against intestinal injury in necrotizing enterocolitis (NEC), mainly through to alleviate inflammation response. The M1 macrophages can promote inflammation. We hypothesized that hydrogen would promote the M1 macrophages conversion during the polarization and reduce the inflammatory factors in NEC. We used M1 and M2 macrophages induced from RAW264.7 cells and bone marrow-derived macrophages, models of NEC and macrophages derived from spleens, abdominal lymph nodes and lamina propria in model mice. Cytokines, CD16/32 and CD206 were measured by quantitative PCR, flow cytometry. Nuclear factor-κB (NF-κB) p65 were determined by western blot. Histology staining were used to assess the severity of NEC. Macrophages were successfully polarized to M1 or M2 by assessing the expression of inflammatory factors. Pro-inflammatory factors and CD16/32 in M1 macrophages were decreased, and the expression of CD16/32 in lamina propria were inhibited after treatment with hydrogen, but the changes has no effects in other tissues. Hydrogen inhibited the NF-κB p65 in M1 macrophages nucleus and distal ileum of NEC. HE staining showed hydrogen could attenuate the severity of NEC. Hydrogen could attenuate the severity of NEC through promoting M1 macrophages conversion by inhibited the expression of NF-κB p65 in the nucleus.

摘要

氢气对坏死性小肠结肠炎(NEC)的肠道损伤具有保护作用,主要是通过减轻炎症反应。M1巨噬细胞可促进炎症。我们推测氢气会在极化过程中促进M1巨噬细胞的转化,并减少NEC中的炎症因子。我们使用了由RAW264.7细胞和骨髓来源的巨噬细胞诱导的M1和M2巨噬细胞、NEC模型以及模型小鼠脾脏、腹腔淋巴结和固有层来源的巨噬细胞。通过定量PCR、流式细胞术检测细胞因子、CD16/32和CD206。通过蛋白质印迹法测定核因子-κB(NF-κB)p65。组织学染色用于评估NEC的严重程度。通过评估炎症因子的表达,巨噬细胞成功极化为M1或M2。氢气处理后,M1巨噬细胞中的促炎因子和CD16/32减少,固有层中CD16/32的表达受到抑制,但其他组织中的变化无影响。氢气抑制了M1巨噬细胞核和NEC远端回肠中的NF-κB p65。苏木精-伊红(HE)染色显示氢气可减轻NEC的严重程度。氢气可通过抑制细胞核中NF-κB p65的表达促进M1巨噬细胞转化,从而减轻NEC的严重程度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/224e/8635714/eb984ae29478/fped-09-710382-g0001.jpg

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