期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 532, 期 4, 页码 555-562出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2020.08.044
关键词
Glycyrrhetinic acid; Acute lung injury; Macrophage; Nlrp3 inflammsome; ROS-PI3K/AKT
资金
- National Natural Science Foundation of China, China [81603587, 81603668]
- National Key Research and Development Program of China, China [2017YFC1700400]
- Guangdong Natural Science Funds for Distinguished Young Scholar [2018B030306027]
- Science and Technology Development Plan of Guangdong Province, China [2017A020211016]
- Youth Medical Talent Fund of Guangzhou University of Chinese Medicine, China [QNYC20170105]
- Science & Technology Award for Young-aged Talents of China Association of Traditional Chinese Medicine [CACM-2017QNRC2-C12]
- Project of Guangzhou University of Chinese Medicine [A1-AFD018171Z11020]
- Fundamental Research Funds for the Central Universities [11616334]
- Famous Chinese Medicine Tradition Studio of Guangdong Province [201805]
Glycyrrhetinic acid (GA), a triterpene saponins, has been widely proven to have multiple medicinal properties. Our study aimed to figure out the protective effect of GA on acute lung injury (ALI) and the underlying mechanism. The LPS-induced ALI model mice were intratracheally administrated with 10 mg/kg LPS. Pretreatment with GA (10, 20, 40 mg/kg, i.g.) ameliorated acute lung injury pathological damage, macrophage infiltration and lung edema. In the lung tissue, immunofluorescence (IF) and Immunohistochemistry (IHC) were performed to detect macrophage Nod-like receptor 3 (Nlrp3) inflammasome activation and interleukin-1 beta (IL-1 beta) protein expression. In macrophages, the co-localization of Nlrp3 with caspase-1 and Nlrp3 with ASC were assessed by IF. The translational and transcriptional level of Nlrp3, cle-caspase-1 and apoptosis-associated speck-like protein containing CARD (ASC), were examined by Western blot and Real time PCR (RT-PCR). The protein expression of Cle-caspase-1 was remarkably suppressed via sh-Nlrp3 transfection compared with LPS groups. GA notably attenuated ALI by inhibiting Nlrp3 formation and activation. Furthermore, GA downregulated the production of reactive oxygen species (ROS) and the phosphorylation level of PI3K and AKT in macrophages. These findings indicate that GA ameliorated ALI in mice by suppressing the activation of Nlrp3 inflammasome which may be mediated by ROS-PI3K/AKT pathway. GA may serve as a promising agent for the attenuation of ALIrelated inflammation and pathology. (C) 2020 The Authors. Published by Elsevier Inc.
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