摘要
目的探讨丹参酮ⅡA对脑缺血-再灌注损伤大鼠的保护作用及其对细胞间黏附分子-1表达及髓过氧化物酶活性的影响。方法80只Wistar大鼠随机分为假手术组、缺血-再灌注组(缺血组)、丹参酮ⅡA小剂量治疗组[小剂量组,15mg/(kg·d)]和丹参酮ⅡA大剂量治疗组[大剂量组,30mg/(kg·d)];线拴法建立局灶性脑缺血-再灌注大鼠模型,治疗组大鼠于手术前连续生理盐水灌胃后给予不同剂量的丹参酮ⅡA。免疫组织化学方法观察脑缺血-再灌注大鼠额顶叶皮质细胞间黏附分子-1表达水平、髓过氧化物酶活性、脑组织含水量及梗死灶体积。结果脑缺血-再灌注后24h,缺血组细胞间黏附分子-1表达阳性的血管数为(63.00±4.74)根/5个高倍视野,髓过氧化物酶活性为(0.42±0.04)U/g,与假手术组[0和(0.03±0.01)U/g]比较,差异有统计学意义(均P<0.01);小剂量组细胞间黏附分子-1表达阳性的血管数为(41.20±4.55)根/5个高倍视野,髓过氧化物酶活性为(0.33±0.02)U/g,大剂量组分别为(26.40±3.78)根/5个高倍视野和(0.23±0.03)U/g,均低于缺血组(P<0.01),两剂量组之间比较差异有统计学意义(P<0.01)。缺血组脑组织含水量为(92.13±2.62)%,梗死灶体积为(194.10±10.99)mm3,与假手术组[(81.09±1.47)%和0]比较差异有统计学意义(均P<0.01);小剂量组脑组织含水量为(87.88±1.86)%,梗死灶体积为(140.86±5.25)mm3,大剂量组分别为(83.36±2.90)%和(112.20±10.78)mm3,均低于缺血组(P<0.01),两剂量组之间比较差异有统计学意义(P<0.01)。结论丹参酮ⅡA对脑缺血-再灌注损伤具有保护作用,其机制可能与缺血-再灌注后细胞间黏附分子-1表达水平和中性粒细胞浸润受到抑制有关。
Objective To study the effects of tanshinone Ⅱ A (Tan Ⅱ A) on the expression of intercellular adhesion molecule-1 (ICAM-I) and myeloperoxidase (MPO) activity of cerebral ischemia- reperfusion (IR) injury in rats. Methods Eighty Wistar rats were randomly divided into 4 groups: sham operated group, IR group, Tan Ⅱ A low dose [15 mg/(kg·d)] group and Tan Ⅱ A high dose [30 mg/(kg·d)] group. The model of focal middle cerebral artery occlusion (MCAO) was developed by suture-occluded method. Rats in Tan ⅡA groups were pretreated before MCAO with saline and assigned dose of Tan ⅡA through gastric peffusion, every day, for 3 d. Rats in sham operated group and IR group were all pretreated with the same volume of saline through gastric perfusion before MCAO. The expression of ICAM-1 in the frontal and parietal cortex of cerebral ischemia-reperfusion rats was detected by immunohistochemistry, and MPO activity was also assessed. Brain water content and cerebral infarction volume were also investigated. Results After 24 h-cerebral ischemia-reperfusion, the number of ICAM-t positive expression vessels was (63.00± 4.74) / 5 high power fields and MPO activity was (0.42± 0.04) U/g in IR group, and there were significant differences in comparison with those in sham operated group [0 and (0.03 ± 0.01 ) U/g] (P〈0.01, for all). In Tan Ⅱ A low and high dose groups, the numbers of ICAM-1 positive expression vessels were (41.20±4.55)/5 high power fields and (26.40± 3.78)/5 high power fields, and the MPO activity were (0.33 ± 0.02) U/g and (0.23 ±0.03) U/g respectively, they were all lower than those in IR group (P〈0.01), and there were significant differences between Tan ⅡA low and high dose group (P〈0.01). The blain water content was (92.13 ±2.62)% and cerebral infarction volume was (194.10±10.99) mm3 in IR group,and there were significant differences in comparison with those in sham operated group [(81.09± 1.47)% and 0] (P〈 0.01, for all). In Tan Ⅱ A low and high dose groups, the brain water content were (87.88 ± 1.86)% and (83.36±2.90)%, and cerebral infarction volume were (140.86 ± 5.25) mm3 and (112.20 ± 10.78) mm3 respectively, they were all lower than those in IR group (P〈0.01), and there were significant differences between Tan Ⅱ A low and high dose group (P 〈 0.01). Conclusion Tanshinone Ⅱ A has protective effect on brain after cerebral ischemia-reperfusion injury. It may be correlated with the inhibiting of inflammatory reaction in cerebral ischemia-reperfusion by decreasing the expression of ICAM-1 and neutrophil infiltration.
出处
《中国现代神经疾病杂志》
CAS
2008年第4期349-352,共4页
Chinese Journal of Contemporary Neurology and Neurosurgery
基金
广西省自然科学基金资助项目(项目编号:0542110)
关键词
丹参酮
再灌注损伤
胞间粘附分子1
过氧化物酶
免疫组织化学
Tanshinone
Reperfusion injury
Intercellular adhesion molecule-l
Peroxidase
Immunohistochemistry