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目的:探讨丁苯酞对实验性自身免疫性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)大鼠的保护作用。方法:健康成年Wistar大鼠40只,随机分为正常组、EAE组、丁苯酞低剂量组[LDG组,100mg/(kg.d)]、丁苯酞高剂量组[HDG组,400mg/(kg.d)],每组10只。建立EAE模型。LDG组、HDG组分别腹腔注射相应剂量的药物。正常组、EAE组仅腹腔注射生理盐水0.5mL/d作为对照。24h后处死大鼠。用Hooper评分评价神经功能;用免疫组织化学方法检测超氧化物歧化酶(SOD)、诱导型一氧化氮合酶(iNOS)的表达水平。取脊髓中腰膨大部分切片HE染色,观察脊髓组织细胞学形态。结果:(1)EAE组神功能缺损程度最严重,丁苯酞干预后,缺损程度明显改善(P<0.05),干预剂量越大,改善越明显。(2)HDG组神经细胞存活数量明显增多,炎性细胞浸润程度最少。(3)EAE组iNOS阳性细胞表达明显升高,SOD表达明显下降,丁苯酞干预后,iNOS表达明显下降,SOD表达明显升高,HDG组变化最明显(P<0.05)。结论:丁苯酞对EAE的保护作用可能与其清除自由基、提高SOD表达及抑制iNOS表达有关。
Objective: To investigate the protective effect of butylphthalide on experimental autoimmune encephalomyelitis (EAE) in rats. Methods: Forty healthy adult Wistar rats were randomly divided into normal group, EAE group, low dose butylphthalide group [LDG group, 100mg / (kg · d)], high dose butylphthalide group [HDG group, 400mg / (kg.d)], 10 in each group. Build an EAE model. LDG group, HDG group were intraperitoneal injection of the corresponding dose of drug. Normal group, EAE group only intraperitoneal injection of saline 0.5mL / d as a control. Rats were sacrificed 24h later. The neurological function was evaluated by Hooper score. The expression of superoxide dismutase (SOD) and inducible nitric oxide synthase (iNOS) was detected by immunohistochemistry. The spinal cord in the lumbar spondylolisthesis HE staining, observed spinal cord cytology. Results: (1) The degree of neurological deficit in EAE group was the most serious. After the injection of butylphthalide, the degree of defect was significantly improved (P <0.05). The greater the intervention dose, the more obvious the improvement was. (2) The number of nerve cells in HDG group increased significantly, and the infiltration of inflammatory cells was the least. (3) The expression of iNOS positive cells increased significantly and the expression of SOD decreased significantly in EAE group. The expression of iNOS decreased obviously and the expression of SOD increased obviously in HDPE group (P <0.05) after butylphthalide treatment. CONCLUSION: The protective effect of butylphthalide on EAE may be related to its ability of scavenging free radicals, increasing the expression of SOD and inhibiting the expression of iNOS.