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髓磷脂碱性蛋白无法预防或抑制豚鼠实验性变应性脑脊髓炎。

Failure of myelin basic protein to prevent or suppress experimental allergic encephalomyelitis in guinea pigs.

作者信息

Hashim G A

出版信息

Neurochem Res. 1980 Feb;5(2):101-13. doi: 10.1007/BF00964325.

DOI:10.1007/BF00964325
PMID:6154252
Abstract

The encephalitogenic myelin basic protein (BP) was reported to be effective in preventing and suppressing the development of experimental allergic encephalomyelitis (EAE) when animals were treated before or after encephalitogenic challenge, respectively. In this report we show that pretreatment with 15 daily doses of 2.5 or 0.15 mg homologous BP (in IFA) failed to protect guinea pigs from subsequent challenge with encephalitogenic emulsion. Similarly, 15 daily injections of 1.0, 2.5, 5.0, or 10.0 mg guinea pig BP (in IFA) did not suppress development of or arrest ongoing EAE when the treatment was initiated on days 1, 4, 8, or 11 after an encephalitogenic challenge. The results show that over 50% of the treated animals developed hind leg paralysis (HLP), incontinence, or both, and the incidence of HLP was not altered significantly by a 10-fold increase in the amount of BP used for daily treatment. Further, all the treated and challenged animals developed histological lesions characteristic of disease. Treatment with BP delayed disease onset, prolonged the period of paralysis leading to recovery from HLP, and reduced both the prevelence of histological lesions as well as the incidence of death. It may be concluded that under these experimental conditions the administration of BP failed to protect from or suppress development of EAE.

摘要

据报道,当动物在致脑炎攻击之前或之后分别接受治疗时,致脑炎的髓鞘碱性蛋白(BP)在预防和抑制实验性变应性脑脊髓炎(EAE)的发展方面是有效的。在本报告中,我们表明,每天15次给予2.5或0.15毫克同源BP(在不完全弗氏佐剂中)进行预处理,未能保护豚鼠免受随后致脑炎乳剂的攻击。同样,当在致脑炎攻击后的第1、4、8或11天开始治疗时,每天15次注射1.0、2.5、5.0或10.0毫克豚鼠BP(在不完全弗氏佐剂中)也不能抑制EAE的发展或阻止其进展。结果显示,超过50%的治疗动物出现后腿麻痹(HLP)、大小便失禁或两者皆有,并且用于每日治疗的BP量增加10倍并未显著改变HLP的发生率。此外,所有接受治疗并受到攻击的动物都出现了疾病特征性的组织学病变。BP治疗延迟了疾病发作,延长了导致从HLP恢复的麻痹期,并减少了组织学病变的发生率以及死亡率。可以得出结论,在这些实验条件下,给予BP未能预防或抑制EAE的发展。

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