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疏风解毒胶囊通过激活NRF2相关抗氧化途径保护大鼠免受脂多糖诱导的急性肺损伤。

Shufeng Jiedu capsules protect rats against LPS-induced acute lung injury via activating NRF2-associated antioxidant pathway.

作者信息

Liao Qingwu, Chen Wenan, Tong Zhufeng, Xue Mingming, Gu Tianwen, Yuan Ying, Song Zhenju, Tao Zhengang

机构信息

Department of Anesthesia, Zhongshan Hospital, Fudan University, Shanghai, China.

Emergency Department, Zhongshan Hospital, Fudan University, Shanghai, China.

出版信息

Histol Histopathol. 2021 Mar;36(3):317-324. doi: 10.14670/HH-18-293. Epub 2020 Dec 21.

Abstract

Shufeng Jiedu capsule (SFJDC) is a traditional Chinese medicine, which has been used for the treatment of respiratory infections for more than thirty years in Hunan (China). SFJDC protected rats against LPS-induced acute lung injury (ALI); however, the molecular mechanisms underlying the therapeutic effects of SFJDC remain unclear. Therefore, this study aimed at analyzing the major anti-inflammatory compounds of SFJDC and exploring the underlying molecular mechanisms. SFJDC dissolved in water was fingerprinted by UPLC/Q-TOF. Inflammation response was assessed by histopathological examination and ELISA assay. Arterial blood gases were also analyzed to evaluate the function of rat lungs. The expression levels of Kelch-like ECH-associating protein 1 (Keap1), Nrf2, heme oxygenase-1 (HO1), Cullin 3 (CUL3) and NQO1 were analyzed by Western blotting. Results indicated that SFJDC alleviated inflammation response by reducing the level of inflammatory cytokines, and upregulation of glutathione-S-transferase (GST) and superoxide dismutase (SOD) in lung tissues. Furthermore, SFJDC suppressed LPS-induced upregulation of Keap 1 and CUL3 in rat lungs. The expression of NRF2 HO1 and NQO1 were further upregulated by SFJDC in the presence of LPS, indicating that SFJDC might activate the NRF2-associated antioxidant pathway. In conclusion, SFJDC treatment may protect the rat lungs from LPS by alleviating the inflammation response via NRF2-associated antioxidant pathway.

摘要

疏风解毒胶囊(SFJDC)是一种中药,在中国湖南已用于治疗呼吸道感染三十多年。SFJDC可保护大鼠免受脂多糖(LPS)诱导的急性肺损伤(ALI);然而,SFJDC治疗作用的分子机制仍不清楚。因此,本研究旨在分析SFJDC的主要抗炎化合物并探索其潜在的分子机制。采用超高效液相色谱/四极杆飞行时间质谱联用仪(UPLC/Q-TOF)对溶解于水中的SFJDC进行指纹图谱分析。通过组织病理学检查和酶联免疫吸附测定(ELISA)评估炎症反应。还分析动脉血气以评估大鼠肺功能。通过蛋白质免疫印迹法分析kelch样ECH相关蛋白1(Keap1)、核因子E2相关因子2(Nrf2)、血红素加氧酶-1(HO1)、Cullin 3(CUL3)和醌氧化还原酶1(NQO1)的表达水平。结果表明,SFJDC通过降低炎症细胞因子水平以及上调肺组织中谷胱甘肽-S-转移酶(GST)和超氧化物歧化酶(SOD)来减轻炎症反应。此外,SFJDC抑制LPS诱导的大鼠肺组织中Keap 1和CUL3的上调。在存在LPS的情况下,SFJDC进一步上调NRF2、HO1和NQO1的表达,表明SFJDC可能激活NRF2相关的抗氧化途径。总之,SFJDC治疗可能通过NRF2相关的抗氧化途径减轻炎症反应,从而保护大鼠肺组织免受LPS损伤。

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