补阳还五汤对脑缺血再灌注损伤大鼠PTEN mRNA的影响

目的:探讨补阳还五汤对脑缺血再灌注大鼠第10号染色体缺失的磷酸酶和张力蛋白同源物基因(PTEN)mRNA表达与血小板活化的影响。方法:将无特定病原体(SPF)级SD大鼠60只随机分为假手术组、模型组、氢氯吡格雷组、补阳还五汤高、低剂量组,每组12只。氢氯吡格雷组ig给予氯吡格雷6.8 mg·kg-1·d-1,补阳还五汤高、低剂量组分别ig给予补阳还五汤26,6.5 g·kg-1·d-1,其余各组ig给予生理盐水,连续给药14 d后,采用大脑中动脉线栓法复制大鼠急性局灶性脑缺血再灌注模型,并在造模前2 h给予相应ig处理,造模60 min后拔除栓线再灌注12 h后收集相应标本保存,测定各组大鼠血浆P-选择素(CD62P)含量与海马组织PTEN mRNA表达情况。结果:与假手术组比较,模型组神经行为评分显著增加,与模型组比较,各用药组的神经行为评分显著降低;与假手术组比较,模型组血浆中CD62P表达显著升高(P0.05);与模型组比较,补阳还五汤组与氢氯吡格雷组均能显著抑制血浆中CD62P表达(P0.05),但补阳还五汤组与氢氯匹格雷组之间抑制作用无显著性差异;与假手术组比较,模型组PTEN mRNA表达显著增加;与模型组比较,各用药组的PTEN mRNA表达显著降低(P0.05),以补阳还五汤高剂量组尤为明显。结论:补阳还五汤对急性脑缺血再灌注损伤模型大鼠的保护机制可能与下调PTEN基因过表达及抑制CD62P表达有关。

Effect of Buyang Huanwu Tang on Expression of PTEN mRNA in Rat Model with Cerebral Ischemia-reperfusion Injury

Objective: To investigate the effect of Buyang Huanwu Tang(BYHWT) on the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) mRNA and platelet activation in rat models with cerebral ischemia-reperfusion injury. Method: Sixty specific pathogen free (SPF) Sprague-Dawley rats (weighing 250-300 g) were randomly divided into 5 groups as following:sham-operated group, clopidogrel group, high-dose BYHWT group, low-dose BYHWT group, and model group, 12 rats in each group. The high-dose BYHWT group and the low-dose BYHWT group were ig administered with 26, 6.5 g·kg^-1·d^-1 BYHWT respectively while the clopidogrel group was ig administered with 6.8 mg·kg^-1·d^-1. Another two groups were ig administered with normal saline. After treatment of the animals for 14 days,middle cerebral artery occlusion method was used to establish models of transient focal cerebral ischemia and reperfusion, and corresponding ig treatment was provided 2 h before modeling. The plugging wire was removed after modeling for 60 min and reperfusion for 12 h before samples collection for determination of the content of P-selection(CD62P) in plasma and expression of PTEN mRNA in hippocampus. Result: The neurological score in model group was significantly higher than that in sham-operated group, and the neurological scores in various treatment groups were significantly lower than that in model group.The expression of CD62P in the model group was significantly higher than that in sham-operated group (P<0.05). BYHWT groups and clopidogrel group can significantly inhibit the expression of CD62P (P<0.05), but without significant difference between BYHWT groups and clopidogrel group. PTEN mRNA expression in model group was significantly higher than that in sham-operated group. PTEN mRNA expression in various treatment groups were significantly lower than that in model group (P<0.05), mostly significant in BYHWT high dose group. Conclusion: The neuroprotective mechanism of BYHWT on acute cerebral ischemia model may relate with down-regulating the expression of PTEN gene over-expression and inhibiting expression of CD62P.