Dexmedetomidine attenuates acute kidney injury induced by hemorrhagic shock/resuscitation in rats / 中国病理生理杂志

AIM:To investigate the effects of dexmedetomidine on hemorrhagic shock /resuscitation(HS/R)-induced acute kidney injury(AKI)in rats,and to explore the possible mechanisms.METHODS:Wistar rats(n=32) were randomly divided into 4 groups(n =8): normal saline control group(NS group), dexmedetomidine group(D group),HS/R group and HS/R+D group.The animals were sacrificed at 6 h after resuscitation.The levels of serum creatinine(Cr)and blood urine nitrogen(BUN)were examined.The kidneys of all rats were removed for evaluation of histological characteristics,and the levels of malondialdehyde(MDA),tumor necrosis factor-α(TNF-α),interleukin-1β (IL-1β)and superoxide dismutase(SOD)were measured.The expression of nuclear factor-κB(NF-κB)and hemeoxyge-nase-1(HO-1)was determined by Western blot.RESULTS: Compared with NS group, the levels of Cr, BUN, MDA, TNF-αand IL-1βwere obviously increased in HS/R group, which were obviously decreased in HS/R+D group(P<0.05).Compared with NS group,the SOD activity was obviously decreased in HS/R group,which was obviously increased in HS/R+D group(P<0.05).Compared with NS group, the protein expression of NF-κB was obviously increased in HS/R group,which was obviously decreased in HS/R+D group(P<0.05).Compared with NS group, the protein ex-pression of HO-1 was increased in HS/R group.Compared with HS/R group,the protein expression of HO-1 was obviously increased in HS/R+D group.Compared with NS group,HS/R induced marked kidney histological injury,which was less pronounced in HS/R+D group.CONCLUSION:Dexmedetomidine effectively protects rats against AKI caused by HS /R, and its mechanism may be associated with the increase in HO-1 expression and the inhibition of NF-κB expression.

Lipoxin A4 Ameliorates Lipopolysaccharide-Induced A549 Cell Injury through Upregulation of N-myc Downstream-Regulated Gene-1 / 中华医学杂志(英文版)

<p><b>Background</b>Lipoxin A4 (LXA4) can alleviate lipopolysaccharide (LPS)-induced acute lung injury (ALI) and acute respiratory distress syndrome through promoting epithelial sodium channel (ENaC) expression in lung epithelial cells. However, how LXA4 promote ENaC expression is still largely elusive. The present study aimed to explore genes and signaling pathway involved in regulating ENaC expression induced by LXA4.</p><p><b>Methods</b>A549 cells were incubated with LPS and LXA4, or in combination, and analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) of ENaC-α/γ. Candidate genes affected by LXA4 were explored by transcriptome sequencing of A549 cells. The critical candidate gene was validated by qRT-PCR and Western blot analysis of A549 cells treated with LPS and LXA4 at different concentrations and time intervals. LXA4 receptor (ALX) inhibitor BOC-2 was used to test induction of candidate gene by LXA4. Candidate gene siRNA was adopted to analyze its influence on A549 viability and ENaC-α expression. Phosphoinositide 3-kinase (PI3K) inhibitor LY294002 was utilized to probe whether the PI3K signaling pathway was involved in LXA4 induction of candidate gene expression.</p><p><b>Results</b>The A549 cell models of ALI were constructed and subjected to transcriptome sequencing. Among candidate genes, N-myc downstream-regulated gene-1 (NDRG1) was validated by real-time-PCR and Western blot. NDRG1 mRNA was elevated in a dose-dependent manner of LXA4, whereas BOC-2 antagonized NDRG1 expression induced by LXA4. NDRG1 siRNA suppressed viability of LPS-treated A549 cells (treatment vs. control, 0.605 ± 0.063 vs. 0.878 ± 0.083, P = 0.040) and ENaC-α expression (treatment vs. control, 0.458 ± 0.038 vs. 0.711 ± 0.035, P = 0.008). LY294002 inhibited NDRG1 (treatment vs. control, 0.459 ± 0.023 vs. 0.726 ± 0.020, P = 0.001) and ENaC-α (treatment vs. control, 0.236 ± 0.021 vs. 0.814 ± 0.025, P < 0.001) expressions and serum- and glucocorticoid-inducible kinase 1 phosphorylation (treatment vs. control, 0.442 ± 0.024 vs. 1.046 ± 0.082, P = 0.002), indicating the PI3K signaling pathway was involved in regulating NDRG1 expression induced by LXA4.</p><p><b>Conclusion</b>Our research uncovered a critical role of NDRG1 in LXA4 alleviation of LPS-induced A549 cell injury through mediating PI3K signaling to restore ENaC expression.</p>

The application of mask oxygen supply in propofol-sedated gastroscopy / 中华消化杂志

0.05).Conclusion The application of oxygen inhalation with a special facial mask during propofol-sedated gastroscopy appears to be more safer than that of oxygen inhalation via snuffle tube.