====== Wortmannin ====== The aim of a [[study]] of Ji and Wang from the [[Cangzhou Central Hospital]], was to investigate the role of μ-[[opioid receptor]]s in [[acute respiratory distress syndrome]] and whether their protective effect is mediated via [[PI3K/AKT/mTOR pathway]]. What is the main finding and its importance? The findings show that activation of μ-opioid receptors ameliorates [[lung injury]], effects reversed by the PI3K inhibitor, [[wortmannin]]. The main pathology of acute respiratory distress syndrome (ARDS) is the accumulation of inflammatory cells in the [[lung]] and increased permeability of vascular [[endothelial cell]]s. The μ-opioid receptor (MOR) is a [[G protein coupled receptor]], which stimulates [[angiogenesis]] and vascular endothelial cell proliferation. In addition, MOR inhibited [[cell]] [[apoptosis]] via PI3K/Akt signaling pathway. In this study, they aimed to explore the contribution of MOR in ARDS and whether effects are mediated via PI3K/Akt signalling. An ARDS model was established by intra-tracheal instillation of 5 mg k-1 g [[lipopolysaccharide]] (LPS). Lung injury was confirmed by [[hematoxylin]] and eosin staining, lung wet/dry weight ratio, bronchoalveolar lavage fluid (BALF) protein concentrations, [[myeloperoxidase]] (MPO) activity and vascular cell adhesion molecule 1 (VCAM-1) expression. Lung inflammation was determined by assessment of [[interleukin]]-1beta (IL-1β) and tumor necrosis factor alpha (TNF-α) concentrations. The protein levels of p-Akt was detected by [[western blot]]. Endomorphin-1-activated MORs attenuated LPS-induced lung injury, lung wet/dry weight ratio, BALF protein concentrations, MPO activity, IL-1β and TNF-α levels and VCAM-1 expression, and elevated LPS-induced decreased p-Akt expression. However, the protective effect of MOR activation on lung injury was reversed by the PI3K inhibitor, wortmannin. In conclusion, μ-opioid receptor involvement in LPS-induced ARDS is via the PI3K/Akt pathway ((Ji S, Wang L. The role of μ-opioid receptors in respiratory distress syndrome μ-opioid receptor signalling via PI3K/Akt pathway ameliorates lipopolysaccharide-induced acute respiratory distress syndrome. Exp Physiol. 2019 Jul 4. doi: 10.1113/EP087783. [Epub ahead of print] PubMed PMID: 31272134. )). ===== Unclassified ===== 2: Xia L, Zhu X, Zhao Y, Yang G, Zuo X, Xie P, Chen C, Han Q. Genome-wide RNA sequencing analysis reveals that IGF-2 attenuates memory decline, oxidative stress and amyloid plaques in an Alzheimer's disease mouse model (AD) by activating the PI3K/AKT/CREB signaling pathway. Int Psychogeriatr. 2019 Jul 3:1-13. doi: 10.1017/S1041610219000383. 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