[ ABSTRACT] AIM:To investigate the effect of adipolin/CTRP12 in LPS-induced acute respiratory distress syn-drome (ARDS) and its potential regulation on alveolar epithelial sodium channel (ENaC) in mice.METHODS:C57BL/6J mice (n=40) were randomly divided into control group, LPS group, adipolin group and wortmannin (PI3K inhibitor) group with 10 mice in each group using random number table.The pathological changes of the lung tissues were evaluated by HE staining.The alveolar fluid clearance ( AFC) was measured by Evans blue-marked albumin, and the concentrations of total protein in bronchoalveolar lavage fluid ( BALF) were assessed by bicinchoninic acid ( BCA) method.In BALF, the levels of IL-1βand TNF-αwere determined by ELISA, and the activity of myeloperoxidase ( MPO) was detected by an MPO assay kit.The total cell counts and polymorphonuclear neutrophil ( PMN) counts in the BALF were analyzed by Gi-emsa staining.The mRNA levels of α-ENaC were assessed by qPCR, while the protein levels of α-ENaC and p-Akt were determined by Western blot.RESULTS: Compared with control group, the classic ARDS pathological changes were ob-served in the mice in LPS group, manifesting by severe pathological lung injury (P<0.05), increases in W/D weight rati-o, total protein levels, cell counts, MPO activitiy, and IL-1βand TNF-αlevels in the BALF, and decrease in AFC ( P<
0.05), accompanied by down-regulated levels of α-ENaC and p-Akt in the lung tissues (P<0.05).The deteriorating effects triggered by LPS were significantly reversed by administration of adipolin.However, PI3K inhibitor wortmannin can-celed the beneficial effects of adipolin on LPS-induced ARDS, as evidenced by aggravated lung injury, increased levels of W/D weight ratio, protein levels, cell counts, MPO activity, and IL-1βand TNF-αlevels in the BALF (P<0.05), and decreased levels of AFC,α-ENaC and p-Akt in the lung tissues.CONCLUSION:Adipolin protects against LPS-induced ARDS in the mice by up-regulatingα-ENaC and enhancing AFC via PI3K/Akt signal pathway.

Objective To investigate the effect of resveratrol on alveolar epithelial sodium channel in acute lung injury mice and the potential mechanism.Methods Twenty-four C57BL/6 mice were randomly divided into control group, LPS group, RES group and PP242(mTORC inhibitor) group with 6 mice in each group.The pathological changes in lung tissue were evaluated by HE staining;the concentrations of total protein in bronchoalveolar lavage fluid (BALF) were assessed by BCA (bicinchoninic acid).The levels of inflammatory cytokines in BALF were determined by ELISA.The proportions of polymorphonuclear neutrophil (PMN) in BALF were detected by Flow Cytometry.The transcription levels of α-ENaC mRNA were assessed by qPCR while the protein levels of α-ENaC and p-GSK1 were measured by Western blot.Results 1)Compared with mice in control group, severe pathological lung injury changes were observed in mice of LPS group, with increased total protein levels, PMN proportions,levels of inflammatory cytokines in BALF (P<0.05), accompanied by down-regulated level of α-ENaC and p-SGK1 in lung tissues (P<0.05).2)Compared with mice in LPS group, resveratrol significantly reversed lung injury triggered by LPS, decreased total protein levels, PMN proportions, levels of inflammatory cytokines in BALF (P<0.05), with down-regulated levels of α-ENaC and p-SGK1 in lung tissues (P<0.05).3)However, PP242 prevented beneficial effects of RES on ALI.Conclusions Up-regulation of α-ENaC expression via activation of SGK1 takes part in the protective effects of RES on LPS-induced ALI in mice.