Haraoui B, Wilder R L, Allen J B, Sporn M B, Helfgott R K, Brinckerhoff C E
Int J Immunopharmacol. 1985;7(6):903-16. doi: 10.1016/0192-0561(85)90054-2.
We studied the effects of oral administration of the retinoid, 4-hydroxyphenyl retinamide (4-HPR), on group A streptococcal cell wall-induced polyarthritis in the rat, a model characterized initially by exudative inflammation of peripheral joints followed by chronic proliferative/erosive synovitis. Experimental arthritis was induced in female LEW/N rats by i.p. injection of streptococcal cell walls in saline (15 micrograms/g body weight). Depending upon the experiment, continuous daily oral administration of the retinoid was begun either 14 days prior to induction of the disease, at the time of cell wall administration and/or 11 days and 31 days after cell wall injection. Dosage was either 1 or 2 mmol 4-HPR/kg of chow. During the course of the disease, severity of clinical illness was assessed by determination of clinical severity index, by histological or radiologic examination, and by measurement of production in vitro of collagenase and prostaglandin E2 by excised synovial tissue. In rats fed the retinoid prior to cell wall injection, both the acute and the chronic responses were suppressed. In rats given the retinoid at the time of cell wall injection, the acute inflammatory response was only partially suppressed on the diet containing 2 mmol 4-HPR/kg chow, but the chronic disease was impressively inhibited in a dose dependent manner. Similarly, in animals with established disease, the drug was also effective; however, the more advanced the illness, the less effective the drug. Clinical observations were paralleled by the histological, radiographical and biochemical analyses. Treated animals showed far less synovial proliferation and joint destruction, and synovial tissues taken from these rats produced lesser amounts of collagenase and prostaglandin E2. No significant toxicity of the retinoid was noted. We conclude that oral administration of 4-HPR suppresses, in a dose and time dependent manner, both the acute and chronic stages of streptococcal cell wall-induced arthritis in rats without apparent significant toxicity. Our data suggest that studies of the effects of this retinoid on patients with chronic inflammatory synovitis are warranted.
我们研究了口服维甲酸4-羟基苯基维甲酰胺(4-HPR)对大鼠A组链球菌细胞壁诱导的多关节炎的影响,该模型最初的特征是外周关节出现渗出性炎症,随后发展为慢性增殖性/侵蚀性滑膜炎。通过腹腔注射溶于生理盐水的链球菌细胞壁(15微克/克体重),在雌性LEW/N大鼠中诱导实验性关节炎。根据实验情况,维甲酸的连续每日口服给药在疾病诱导前14天开始,或在给予细胞壁时开始,和/或在细胞壁注射后11天和31天开始。剂量为1或2毫摩尔4-HPR/千克食物。在疾病过程中,通过测定临床严重程度指数、组织学或放射学检查以及通过测量切除的滑膜组织体外产生胶原酶和前列腺素E2的量来评估临床疾病的严重程度。在细胞壁注射前喂食维甲酸的大鼠中,急性和慢性反应均受到抑制。在给予细胞壁时给予维甲酸的大鼠中,在含有2毫摩尔4-HPR/千克食物的饮食中,急性炎症反应仅部分受到抑制,但慢性疾病以剂量依赖性方式受到显著抑制。同样,在患有已确诊疾病的动物中,该药物也有效;然而,疾病越严重,药物效果越差。临床观察结果与组织学、放射学和生化分析结果一致。接受治疗的动物滑膜增殖和关节破坏明显减少,并且从这些大鼠获取的滑膜组织产生的胶原酶和前列腺素E2量较少。未观察到维甲酸有明显毒性。我们得出结论,口服4-HPR以剂量和时间依赖性方式抑制大鼠链球菌细胞壁诱导的关节炎的急性和慢性阶段,且无明显显著毒性。我们的数据表明,有必要研究这种维甲酸对慢性炎症性滑膜炎患者的影响。