SD大鼠和Wistar大鼠实验性自身免疫性脑脊髓炎发病情况比较

目的比较Wistar大鼠和Sprague-Dawley（SD）大鼠实验性自身免疫性脑脊髓炎（EAE）发病情况。方法注射以豚鼠脊髓匀浆-完全福氏佐剂制备的完全抗原,辅以百日咳疫苗加强诱导,复制Wistar大鼠和SD大鼠EAE模型,比较两组大鼠EAE的神经症状及中枢神经不同部位病理学改变。结果Wistar大鼠组发病数、潜伏期、发病达峰时间以及神经症状最高评分分别为9/12、12.33±1.37、15.17±3.19、1.33±0.41;SD大鼠组分别为11/12、15.88±0.64、18.63±1.52、3.13±1.89;两组大鼠相比,SD大鼠EAE潜伏期延长（P〈0.01）,达峰时间相应推迟（P〈0.05）,但神经症状较Wistar大鼠严重（P〈0.05）;病理结果显示,两组大鼠CNS均以脑干病理改变最为严重,而大脑病变最轻,SD大鼠总体中枢系统炎症改变较Wistar大鼠严重（标准评分P〈0.01,血管套计数P〈0.05）。结论SD大鼠EAE与Wistar大鼠EAE比较,发病过程很相似：发病率接近,中枢炎症病理改变相仿,两者均以脑干炎症变化最严重;略有不同点是：SD大鼠EAE发病潜伏期较长（P〈0.01）,神经症状较严重（P〈0.05）,总体中枢炎症改变较为严重。故SD大鼠也是制备EAE模型的理想实验动物。

Comparison of the Pathogenesis of Experimental Autoimmune Encephalomyelitis in Sprague-Dawley and Wistar Rats

Objective To compare the development rule and inflammatory response of experimental autoimmune encephalomyelitis （EAE）,an animal model of autoimmune disease multiple sclerosis, in Sprague-Dawley （SD） rats and Wistar rats. Methods Twelve adult female Wistar rats and SD rats were utilized for the present experiments. The EAE model was induced by injecting emulsified spinal cord homogenate of guinea-pig （GPSCH） with complete Freud＇s adjuvant （CFA） and intraperitoneal injecting Bordetella pertussis vaccine. After immunization the rats were weighed and evaluated twice daily for clinical signs of EAE. At the acute phase of EAE, EAE-suffering rats which got a maximal clinical scores were euthanized and samples of brain and spinal tissues from different sites were dissected for assessing the degree of inflammatory infiltration. The clinical symptoms and pathological changes of central nervous system were compared between the two strains of rats. Results Most of the Wistar and SD rats （9/12 and 11/12, respectively） injected with GPSCH developed typical EAE and got serious clinical symptoms during the peak-time of disease. Just as expected, the body weight of EAE-suffering rats decreased rapidly as clinical signs became severe. The differences of incidence between the two strains of rats showed to be statistically not significant （P 〉 0.05）. Interestingly,the latency and peak time of EAE in SD rats were longer （15.88 ± 0.64d, P 〈 0.01 and 18.63 ± 1.52d, P 〈 0.05, respectively） and the maximal clinical score in SD rats was higher （3.13± 1.89, P 〈 0.05 ） compared with those in Wistar rats. The pathological examination showed that brainstem in both strains of rats suffered the most severe lesions among all sites of CNS, but cerebrum got the slightest nervous damage. Significant inflammatory infiltration of mononuclear cells, confluent demyelination around blood vessels and typical perivascular cuffing were observed in the brainstem of these EAE-suffering animals. Consistent with the differences of clinical signs between the two strains of rats, the nervous inflammatory lesions of CNS in SD rats were more serious （2.83 ± 1.48 as standard pahological score, P 〈 0.05） than that in Wistar rats, in general. A statistically significant positive correlation between the clinical score and the standard pathological score is apparent from Spearman＇s rho values （7 = 0.714, P 〈 0.05 for Wistar rats; 7 = 0.680, P 〈 0.05 for SD rats）, reflecting the validity of the pathological score. Conclusion The development of EAE and the inflammatory response are most serious in the brainstem, and similar in rats of the two strains. However, in SD rats, the maximal clinical score is higher, and the inflammatory response is more serious than that in Wistar rats. It is concluded that SD rats are also ideal animals for establishing EAE model, and are the more suitable animals for exploring the pathologic mechanism of EAE than wistar rats.