EFFECTS OF THE ANGIOTENSIN-CONVERTING ENZYME-INHIBITOR CAPTOPRIL ON EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
EFFECTS OF THE ANGIOTENSIN-CONVERTING ENZYME-INHIBITOR CAPTOPRIL ON EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
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DOI：
10.3109/08923979509016382
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发表时间：
1995-01-01
影响因子：
3.3
通讯作者：
ROSTAMI, A
中科院分区：
文献类型：
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作者：
CONSTANTINESCU, CS;VENTURA, E;ROSTAMI, A
血管紧张素转换酶（ACE）(1)介导炎症，参与某些抗原肽对T细胞的刺激，并影响血脑屏障（BBB）的通透性。多发性硬化症（MS）是一种中枢神经系统（CNS）的自身免疫性疾病，其特征是血脑屏障通透性增加。ACE抑制剂卡托普利抑制某些免疫功能，抑制炎症或自身免疫性疾病。我们研究卡托普利对多发性硬化症动物模型Lewis大鼠EAE的影响，14只EAE大鼠从免疫到刺激后21天每天给予卡托普利30 mg/kg，并与14只未给药的大鼠进行比较。测量严重程度评分和淋巴细胞对髓鞘碱性蛋白和丝裂原的反应性。卡托普利治疗组与未治疗组的平均和累积临床评分差异有统计学意义（p < 0.05）。卡托普利治疗EAE大鼠的淋巴细胞在疾病严重程度高峰时对MBP和豆豆蛋白a的反应减弱，数据表明卡托普利对Lewis大鼠EAE有显著的有益作用。进一步的研究包括其他ACE抑制剂或其他具有免疫、炎症或血脑屏障作用的肽酶抑制剂，可能会发现潜在有价值的免疫药理学药物。
Angiotensin converting enzyme (ACE)(1) mediates inflammation, participates in T cell stimulation by certain antigenic peptides, and influences the permeability of the blood brain barrier (BBB). ACE is elevated in multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), characterized by increased BBB permeability. ACE inhibitor captopril suppresses certain immune functions and inhibits inflammatory or autoimmune diseases. We studied the effect of captopril on Lewis rat EAE, an animal model of MS. Fourteen rats with EAE were treated with captopril 30 mg/kg daily from immunization to day 21 postimmunization, and compared with 14 untreated rats. Severity scores and lymphocyte reactivity to myelin basic protein and mitogen were measured. There was a statistically significant (p < 0.05) difference between the mean and cumulative clinical scores of captopril-treated and untreated animals. Lymphocytes from captopril treated EAE rats at the peak of disease severity had diminished responses to MBP and concanavalin A. The data suggest a significant beneficial effect of captopril in Lewis rat EAE. Further studies including other inhibitors of ACE or of other peptidases with immune, inflammatory or BBB role, may identify potentially valuable immunopharmacologic agents.