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Attenuation of Lipopolysaccharide-Induced Acute Lung Injury by Hispolon in Mice, Through Regulating the TLR4/PI3K/Akt/mTOR and Keap1/Nrf2/HO-1 Pathways, and Suppressing Oxidative Stress-Mediated ER Stress-Induced Apoptosis and Autophagy

1
Graduate Institute of Aging Medicine, School of Medicine, China Medical University, Taichung 404, Taiwan
2
Department of Health and Nutrition Biotechnology, Asia University, Taichung 413, Taiwan
3
Graduate Institute of Biomedical Sciences, School of Medicine, China Medical University, Taichung 404, Taiwan
4
Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, College of Chinese Medicine, China Medical University, Taichung 404, Taiwan
*
Author to whom correspondence should be addressed.
These authors contributed equally to the work.
Nutrients 2020, 12(6), 1742; https://doi.org/10.3390/nu12061742
Received: 14 May 2020 / Revised: 5 June 2020 / Accepted: 8 June 2020 / Published: 10 June 2020
(This article belongs to the Section Phytochemicals and Human Health)
The anti-inflammatory effect of hispolon has identified it as one of the most important compounds from Sanghuangporus sanghuang. The research objectives were to study this compound using an animal model by lipopolysaccharide (LPS)-induced acute lung injury. Hispolon treatment reduced the production of the pro-inflammatory mediator NO, TNF-α, IL-1β, and IL-6 induced by LPS challenge in the lung tissues, as well as decreasing their histological alterations and protein content. Total cell number was also reduced in the bronchoalveolar lavage fluid (BALF). Moreover, hispolon inhibited iNOS, COX-2 and IκB-α and phosphorylated IKK and MAPK, while increasing catalase, SOD, GPx, TLR4, AKT, HO-1, Nrf-2, Keap1 and PPARγ expression, after LPS challenge. It also regulated apoptosis, ER stress and the autophagy signal transduction pathway. The results of this study show that hispolon regulates LPS-induced ER stress (increasing CHOP, PERK, IRE1, ATF6 and GRP78 protein expression), apoptosis (decreasing caspase-3 and Bax and increasing Bcl-2 expression) and autophagy (reducing LC3 I/II and Beclin-1 expression). This in vivo experimental study suggests that hispolon suppresses the LPS-induced activation of inflammatory pathways, oxidative injury, ER stress, apoptosis and autophagy and has the potential to be used therapeutically in major anterior segment lung diseases. View Full-Text
Keywords: hispolon; anti-inflammation; apoptosis; LPS; HO-1; Nrf-2; ER stress hispolon; anti-inflammation; apoptosis; LPS; HO-1; Nrf-2; ER stress
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Huang, C.-Y.; Deng, J.-S.; Huang, W.-C.; Jiang, W.-P.; Huang, G.-J. Attenuation of Lipopolysaccharide-Induced Acute Lung Injury by Hispolon in Mice, Through Regulating the TLR4/PI3K/Akt/mTOR and Keap1/Nrf2/HO-1 Pathways, and Suppressing Oxidative Stress-Mediated ER Stress-Induced Apoptosis and Autophagy. Nutrients 2020, 12, 1742.

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