Regulating Effects Of Shenxiong Huayu Capsule Preconditioning On The Expression Subtype Of NOS In Cerebral Ischemia Reperfusion Injury In Rats

Objectives To observe the expression of different subtypes of NOS(eNOS、nNOS andiNOS)in Rats with cerebral ischemia reperfusion injure. Meanwhile, through thepreconditioning of different doses Shenxiong Huayu capsule to the rats, further discussthe influence of Shenxiong Huayu capsule on the expression of three subtypes NOS andthe mechanism of Shenxiong Huayu capsule on cerebral ischemia reperfusion injury inrats.Methods1150healthy male SD rats were randomly divided into sham-operation group,ischemia reperfusion model group, Shenxiong Huayu capsule high, medium and low dosegroup. And The groups were divided randomly into3h,6h,12h,24h,48h,72h6points in time.2The Shenxiong Huayu capsule high, medium and low dose group wasrespectively intragastric administrated by Shenxiong Huayu capsule low, medium andhigh dose(480,240,120mg.kg-1)7days before the operation. sham-operation group andischemia reperfusion model group were intragastric administrated by the same dosage ofnormal saline. Continuous7d,1times a day.3Middle cerebral artery occlusion (MCAO)reperfusion model was made by the Longas intraluminal filament method. Then assessedthe neurologic deficit score at each time.4The expression of eNOS、nNOS and iNOSwere detectioned by immunohistochemical method.5Statistical treatment: The data wasanalysed through SPSS19.0software, and was epresented as mean±Sd. Significance wastested with the groups designed analysis of single variance. There was statisticallysignificance if P<0.05.Results1Neurological deficit only appeard in model group and Shenxiong Huayucapsule preconditioning group, and it was clearly improved in the Shenxiong Huayucapsule preconditioning group(P<0.05), especially the high dose group showing asignificant difference.2eNOS expressed in sham-operation group, ischemia reperfusion(CI/R)model group, Shenxiong Huayu capsule group.Through the6time points, longerduration of ischemia reperfusion, the expression of eNOS quantity increase gradually,12h to the peak, then gradually declined. Compared with the sham-operation group, theexpression of eNOS was increased in model group at the6time points(P<0.05, orP<0.01). Compared with the model group, eNOS expressed in Shenxiong Huayu capsule group was significantly increased,especially the high dose group showing a significantdifference.3nNOS expressed in sham-operation group, ischemia reperfusion (CI/R)model group, Shenxiong Huayu capsule group. Through the6time points, longerduration of ischemia reperfusion, the expression of nNOS quantity increase gradually,12h to the peak, then gradually declined. Compared with the sham-operation group, theexpression of nNOS was increased in model group at the6time points(P<0.05, orP<0.01). Compared with the model group, nNOS expressed in Shenxiong Huayu capsulegroup was significantly decreased, especially the high dose group showing a significantdifference.4There was no iNOS expressed in sham-operation group, but there was iNOSdetected both in ischemia reperfusion (CI/R)model group and Shenxiong Huayu capsulegroup. Longer duration of ischemia reperfusion, the expression of iNOS quantity increasegradually. Compared with the sham-operation group, the expression of iNOS wassignificantly increased in model group at the6time points(P<0.01). Compared with themodel group, iNOS expressed in Shenxiong Huayu capsule group was significantlydecreased(P<0.05, or P<0.01), especially the high dose group showing a significantdifference.Conclusions1The expression of nitric oxide synthase was involved in the pathologicalprocesses of cerebral ischemia reperfusion injury. eNOS and nNOS expressed at early,then decreased subsequently; iNOS expressed gradually later in the cerebral ischemiareperfusion.2Shenxiong-huayu Capsule had an effect on the expression of NOS. Whichsuggests that Shenxiong-huayu Capsule can ameliorate acute cerebral ischemiareperfusion injury in rats via increasing eNOS and decreasing both nNOS and iNOS.