Baicalin Ameliorates Radiation-Induced Lung Injury by Inhibiting the CysLTs/CysLT1 Signaling Pathway

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作者
Bao, Wu-An [1 ]
Wang, Yue-Zhen [1 ]
Zhu, Xiang [2 ]
Lin, Juan [2 ]
Fan, Ju-Fen [1 ]
Yang, Yang [2 ]
Zhou, Xia [1 ,2 ]
机构
[1] Univ Chinese Acad Sci, Canc Hosp, Zhejiang Canc Hosp, Dept Radiat Therapy, Hangzhou, Zhejiang, Peoples R China
[2] Chinese Acad Sci, Inst Canc & Basic Med IBMC, Hangzhou, Zhejiang, Peoples R China
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R [医药、卫生];
学科分类号
10 ;
摘要
Objective. Radiation-induced lung injury (RILI) is a common complication of radiotherapy for thoracic tumors. This study investigated the alleviating effect of baicalin (BA) on RILI and its possible mechanism. Methods. RILI model was established by chest irradiation (IR) of C57BL/6 mice for 16 weeks. Different concentrations of BA were administered, and dexamethasone (DXM) was used as a positive control. Then, the lung pathological changes were observed by HE and Masson staining. The levels of TGF-beta, TNF-alpha, IL-1 beta, IL-6, CysLT, LTC4, and LTE4 were measured by ELISA. The CysLT1 expression was detected by qPCR, immunohistochemistry, and western blot. Type II AEC cells were pretreated with LTD-4 to establish the RILI cell model and intervened with different concentrations of BA. Then, the collagen I protein level was measured by ELISA. The CysLT1 and alpha-SMA expression were detected by qPCR, immunofluorescence, and western blot. Results. BA could effectively improve lung histopathological changes and pulmonary fibrosis. In vivo, BA could inhibit the levels of TGF-beta, TNF-alpha, IL-1 beta, and IL-6 and reduce the levels of CysLT, LTC4, and LTE4. In vitro, different concentrations of LTD4 could reduce the viability of type II AEC cells, which could be reversed by the administration of different concentrations of BA. In addition, BA could reduce CysLT1 mRNA, as well as CysLT1 and alpha-SMA protein levels in vitro and in vivo. Conclusion. BA attenuated lung inflammation and pulmonary fibrosis by inhibiting the CysLTs/CysLT1 pathway, thereby protecting against RILI.
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页数:10
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