Protective Effects of Kirenol against Lipopolysaccharide-Induced Acute Lung Injury through the Modulation of the Proinflammatory NF kappa B Pathway and the AMPK2-/Nrf2-Mediated HO-1/AOE Pathway

doi:10.3390/antiox10020204

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/23407

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Title:	Protective Effects of Kirenol against Lipopolysaccharide-Induced Acute Lung Injury through the Modulation of the Proinflammatory NF kappa B Pathway and the AMPK2-/Nrf2-Mediated HO-1/AOE Pathway
Authors:	Lin, FCF;Lee, SS;Li, YC;Ho, YC;Chen, WY;Chen, CJ;Lee, MW;Yeh, KL;Tsai, SCS;Kuan, YH
Keywords:	lipopolysaccharide;acute lung injury;kirenol;NF-κ B pathway;AMPK2;Nrf2-mediated HO-1;AOE pathway
Date:	2021
Issue Date:	2022-08-05T09:36:47Z (UTC)
Publisher:	MDPI
Abstract:	Acute lung injury (ALI) is an acute and life-threatening inflammatory disease of the lung parenchyma that is associated with high mortality worldwide. No therapeutic strategies have been developed for the mitigation of the proinflammatory response that characterizes ALI. Kirenol has anti-inflammatory, antiarthritic, and immunoregulatory effects. In the present study, we investigated the protective effects of kirenol against lipopolysaccharides (LPS)-induced ALI in mice. Kirenol reduced the LPS-induced histopathology changes involving edema and thickening of the interstitial or alveolar walls, infiltration of leukocytes, formation of hyaline membrane. Pretreatment with kirenol reduced leukocytes infiltration in bronchoalveolar lavage fluid (BALF), the alveolar-capillary barrier disruption and lipid peroxidation in lung tissues induced by LPS. Kirenol significantly inhibited the secretion of cytokines, IL-1 beta, IL6, and TNF alpha, into the BALF of the mice with LPS-induced ALI through NF kappa B activation. Moreover, kirenol attenuated the downregulation of the antioxidant enzymes, superoxide dismutase, glutathione peroxidase, and catalase that was induced by LPS. HO-1 expression and the phosphorylation of Nrf2 and AMPK2 were also induced by kirenol. The results indicate that kirenol can be developed as a treatment strategy for ALI, and its effects are induced through the inhibition of the NF-kappa B proinflammatory pathway and promotion of AMPK2/Nrf2-mediated HO-1 and antioxidant enzymes (AOE) activation.
URI:	http://dx.doi.org/10.3390/antiox10020204 https://www.webofscience.com/wos/woscc/full-record/WOS:000622020600001 https://ir.csmu.edu.tw:8080/handle/310902500/23407
Relation:	ANTIOXIDANTS ,2021,v10,issue 2
Appears in Collections:	[中山醫學大學研究成果] 期刊論文

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