Investigate The Effect Of Sevoflurane On BSC1 And AQP2 Expression During Renal Ischemia-reperfusion Injury And The Protection Of Sevoflurane On Renal Ischemia Reperfusion Injury In Rats

Objective:To investigate the effect of Sevoflurane on Na~+-2Cl~--K~+co-transporter-1(BSC1)and aquaporins-2 water channel (AQP2)expressionduring renal ischemia-reperfusion injury(IRI) and the protection andmechanism of sevoflurane on renal ischemia reperfusion injury in rats.Methods:SD rats were allocated randomly and equally to operating group(group C), false ischemia reperfusion group(group I/R) , sevofluranereconditioning group(group Spre-c)and sevoflurane postconditioning group(group Spost-c).Every grope were divide into 3 subsets with 5 animales(30min,45min, 60min) according to the time of renal ischemia. All animalswere killed 24 h after ischemia reperfusion injury for histologic examination,Serum urea nitrogen(BUN)and creatinine ( Cr)were detected, superoxidedismutase (SOD) activity , myeloperoxidase (MPO) activity andconcentration of malonaldehyde (MDA) in renal tissue(OSOM+C andISOM+IM)and serum were examined.Collect urine to observe the change ofthe urine volume , urine specific gravity , urine creatinine and creatinineclearance.The levels of BSC1 in renal cortex and AQP2 in renal inner medullawas detected by Real Time RT-PCR,Western blot and immuno- histochemistry.Renal histopathology lesions were examined.Approach the degree of renalinjury.Results:1.The renal function of rats 24h after IRI was significantly differentbetween groups.Rats subjected to showed significant increase in serum Cr andBUN Compared with C group(P<0.05).The renal function changes caused by IRI were significantly improved by Spre-C(30,45 min) and Spost-C(30,45 min)treatments(P<0.05).There were no Significant difference among I/R(60min),Spre-C (60min)and Spost-C(60min) (P>0.05). And there were no significantdifference between Spre-C and Spost-C (p>0.05).in significant down-regulation of the activities of SOD (P<0.05);whilecompared with I/R group(30,45 min),Spre-C (30,45 min)andSpost-C(30,45min) treatments resulted in significant up-regulation of theiractivities(P<0.05); Compared with C group,the IRI rats resulted in significantincreases of the levels of MDA and MPO,While compared with I/Rgroup,Spre-C (30,45 min)and Spost-C(30,45 min) treatments resulted insignificant decreases of the levels of MDA and MPO,There were noSignificant difference among I/R(60min), Spre-C (60min)and Spost-C(60min)(P>0.05). And there were no significant difference between Spre-C andSpost-C (p>0.05).3.Renal lRI resulted in significant renal injury as evidenced by tubularnecrosis medullary hemorrhage,eongestion,and development ofproteinaceous casts.In contrast,treatments of Spre-C(30,45 min) and Spost-C(30,45 min) group ameliorated these severe renal damages.According toPaller's scores,Quantitative analysis showed a dramatically decreased score inboth Spre-C(30,45 min) and Spost-C (30,45 min) group compared withIR(30,45 min) group(P<0.05). There were no Significant difference amongI/R(60min), Spre-C (60min)and Spost-C(60min) (P>0.05). And there were nosignificant difference between Spre-C and Spost-C (p>0.05).4.Compared with C group, the IRI rats resulted in significant increases ofthe volume of urine and decreases of the urine specific gravity , urine creatinineand creatinine clearance.There were no Significant difference among I/R, Spre-C and Spost-C(P>0.05). 5.The Mrna and Protein expression of BSC1 and AQP2 was evaluated byRealTime-PCR,Western blot and immunohistochemistry. Compared with Cgroup,the IRI rats resulted In significant down-regulation of BSC1 andAQP2mRNA and Protein expression in renal(P<0.05); While compared withI/Rgroup,Spre-C (30,45 min)and Spost-C(30,45 min) treatments resulted insignificant up-regulation of BSC1 and AQP2mRNA and protein expression(P<0.05). There were no Significant difference among I/R(60min), Spre-C(60min)and Spost-C(60min) (P>0.05). And there were no significant differencebetween Spre-C and Spost-C (p>0.05).Conelusion1.Sevoflurane preconditioning and postconditioning were effectivelyprotected renal against IRI.2.The fuction and structure of renal tissue were damaged by renal IRI inrats with the decrease of BSC1 and AQP2 Mrna and protein expression.3.Sevoflurane up- regulating the expression of BSC1 and AQP2 inischemia-reperfusion.4.The mechanism of isehemic preconditioning and postconditioningagainst renal IRI maybe associated to up- regulating BSC1 and AQP2 Mrnaand protein expression.