ABSTRACT
Objective To evaluate the effect of dexmedetomidine on the expression of Semaphorin 7A during lung ischemia-reperfusion (I/R) in rats.Methods Thirty healthy clean-grade adult male Sprague-Dawley rats,aged 8-12 weeks,weighing 200-240 g,were divided into 3 groups (n=10 each) using a random number table method:sham operation group (S group),I/R group and dexmedetomidine group (D group).Only sternotomy was performed,and the left hilum of lung was not clamped in S group.The model of lung I/R injury was established by clamping the left hilum of lung for 45 min followed by 120 min of reperfusion in I/R group.Dexmedetomidine 50 μg/kg was intraperitoneally injected at 30 min before ischemia,and then the model was established in D group.The rats were sacrificed at the end of reperfusion,and the lungs were removed for examination of the pathological changes (using haematoxylin and eosin staining) which were scored and for determination of the wet to dry weight ratio (W/D ratio),expression of Semaphorin 7A protein and mRNA (by Western blot or real-time polymerase chain reaction),and contents of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in lung tissues (by enzyme-linked immunosorbent assay).Results Compared with S group,W/D ratio and pathological scores were significantly increased,the expression of Semaphorin 7A protein and mRNA was up-regulated,and the contents of TNF-α and IL-1β were increased in I/R and D groups (P＜0.05).Compared with I/R group,W/D ratio and pathological scores were significantly decreased,the expression of Semaphorin 7A protein and mRNA was down-regulated,and the contents of TNF-α and IL-1 β were decreased in D group (P＜0.05).Conclusion The mechanism by which dexmedetomidine reduces lung I/R injury may be related to down-regulating Semaphorin 7A expression,thus inhibiting inflammatory responses of rats.
ABSTRACT
Objective To investigate the effects of sevoflurane on renal ischemia-reperfusion (I/R) injury in rats and the role of Na+-2Cl--K+ cotransporter 1 (BSC1) and aquaporin 2 (AQP2) in it.Methods Twentyfour male Sprague-Dawley rats,aged 8-12 weeks,weighing 125-145 g,were randomly divided into 3 groups (n =8 each) ∶ sham operation group (S group),I/R group and sevoflurane group (Sev group).Renal ischemia was induced by occlusion of the renal artery for 45 min with atraumatic microclips followed by 24 h reperfusion.In group Sev,the rats inhaled 1 MAC (2.2％) sevoflurane,renal ischemia was induced after loss of consciousness and 1 MAC (2.2％) sevoflurane was inhaled for 1 h.The urine were collected at 24 h before I/R (T1) and 24 h of reperfusion (T2) for detection of urine specific gravity and creatinine (Cr) level.The urine volume was recorded.The endogenous creatinine clearance rate (Ccr) was calculated.Blood samples were taken from the irferior vena cava at T2 for determination of concentrations of serum blood urea nitrogen (BUN) and Cr and activities of superoxide dismutase (SOD) and myeloperoxidase (MPO),malondialdehyde (MDA) concentration.The left kidney was removed for determination of MPO and SOD activities and MDA content and for microscopic examination and the pathological changes of the renal tubule were scored.The expression of AQP2 and BSC1 was detected by immunohistochemistry and Western blot.Results Compared with group S,the urine volume was enlarged,concentrations of serum BUN and Cr were significantly increased,urine specific gravity and Ccr were significantly decreased,MPO and MDA levels were significantly increased,SOD activity was significantly decreased,the pathological score was significantly increased,and the expression of AQP2 and BSC1 was down-regulated in groups I/R and Sev (P ＜ 0.05).Cer was significantly higher,conceutratious of serum BUN and Cr and MPO and MDA levels were lower,SOD activity was higher,the pathological score was lower,and the expression of AQP2 and BSC1 was higher in group Sev than in group I/R (P ＜ 0.05).Sevoflurane inhalation significantly attenuated the pathological changes.Conclusion Sevoflurane can attenuate renal I/R injury in rats through up-regulating the expression of BSC1 and AQP2.