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电针预处理通过减轻炎症和调节巨噬细胞极化来保护脓毒症大鼠免受急性肺损伤。

Electroacupuncture pretreatment protects septic rats from acute lung injury by relieving inflammation and regulating macrophage polarization.

机构信息

Department of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, China.

Key Laboratory of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, China.

出版信息

Acupunct Med. 2023 Jun;41(3):175-182. doi: 10.1177/09645284221118588. Epub 2022 Aug 30.

Abstract

BACKGROUND

Macrophage polarization toward the M2 phenotype may attenuate inflammation and have a therapeutic effect in acute lung injury (ALI).

OBJECTIVE

To investigate the role of electroacupuncture (EA) pretreatment on the inflammatory response and macrophage polarization in a septic rat model of lipopolysaccharide (LPS)-induced ALI.

METHODS

Male Sprague Dawley rats (n = 24) were randomly divided into three groups (n = 8 each): control (Ctrl), ALI (LPS) and pre-EA (LPS + EA pretreatment). ALI and pre-EA rats were injected with LPS via the caudal vein. Pulmonary edema was assessed by left upper pulmonary lobe wet-to-dry (W/D) ratios. Lung injury scores were obtained from paraffin-embedded and hematoxylin and eosin-stained sections of the left lower pulmonary lobe. Inflammatory activation was quantified using serum tumor necrosis factor (TNF)-α, interleukin (IL)-1β, transforming growth factor (TGF)-β and IL-10 levels measured by enzyme linked immunosorbent assay (ELISA). Macrophage phenotype was determined by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting.

RESULTS

Mean lung W/D ratio was significantly lower and serum IL-1β levels were decreased in pre-EA rats compared to ALI rats (P < 0.05). TNF-α mRNA expression was decreased and mannose receptor (MR) and Arg1 mRNA expression was increased in the lung tissues of pre-EA rats compared to ALI rats (P < 0.01). Arg1 protein expression was similarly increased in the lung tissues of pre-EA rats compared to ALI rats (P < 0.05).

CONCLUSION

EA pretreatment may play a protective role by promoting macrophage polarization to the M2 phenotype in a septic rat model of LPS-induced ALI.

摘要

背景

巨噬细胞向 M2 表型极化可能会减轻炎症,并对急性肺损伤 (ALI) 产生治疗作用。

目的

探讨电针预处理在脂多糖 (LPS) 诱导的 ALI 脓毒症大鼠模型中对炎症反应和巨噬细胞极化的作用。

方法

雄性 Sprague Dawley 大鼠 (n = 24) 随机分为三组 (n = 8 只/组):对照组 (Ctrl)、ALI 组 (LPS) 和电针预处理组 (LPS + EA 预处理)。ALI 和电针预处理组大鼠通过尾静脉注射 LPS。通过左肺上叶湿重/干重 (W/D) 比值评估肺水肿。从左下肺叶石蜡包埋和苏木精-伊红染色切片中获得肺损伤评分。通过酶联免疫吸附试验 (ELISA) 测量血清肿瘤坏死因子 (TNF)-α、白细胞介素 (IL)-1β、转化生长因子 (TGF)-β 和 IL-10 水平来量化炎症激活。通过实时定量聚合酶链反应 (RT-qPCR) 和 Western blot 测定巨噬细胞表型。

结果

与 ALI 组相比,电针预处理组大鼠平均肺 W/D 比值显著降低,血清 IL-1β 水平降低 (P < 0.05)。与 ALI 组相比,电针预处理组大鼠肺组织 TNF-α mRNA 表达降低,甘露糖受体 (MR) 和 Arg1 mRNA 表达增加 (P < 0.01)。与 ALI 组相比,电针预处理组大鼠肺组织 Arg1 蛋白表达也增加 (P < 0.05)。

结论

电针预处理可能通过促进巨噬细胞向 LPS 诱导的 ALI 脓毒症大鼠模型中的 M2 表型极化发挥保护作用。

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