Camussi G, Salvidio G, Niesen N, Brentjens J, Andres G
Department of Pathology, State University of New York, Buffalo 14214.
Am J Pathol. 1988 Jun;131(3):418-34.
Chlorpromazine blocks antibody-mediated redistribution of cell surface antigens in vitro and in vivo and inhibits the development of passive Heymann glomerulonephritis, a disease characterized by in situ formation of immune complexes (Camussi et al J Immunol 1986, 136:2127-2135). The aim of this study was to establish whether chlorpromazine exerts similar effects in other rat models characterized by in situ formation of immune complexes. In glomerulonephritis induced by antibodies reactive with an exogenous antigen "planted" in glomeruli pretreatment with chlorpromazine prevented formation of "humps" and exudative and proliferative lesions. Likewise, chlorpromazine prevented passive reverse Arthus reaction in the skin. In contrast, the drug was ineffective when these lesions were already established, and also failed to inhibit the fulminant course of nephrotoxic serum glomerulonephritis with an enhanced autologous phase. It is proposed that the antiinflammatory effect of chlorpromazine is due to its ability to block the recruitment of inflammatory cells and the release of inflammatory mediators.
氯丙嗪在体外和体内均可阻断抗体介导的细胞表面抗原再分布,并抑制被动性海曼肾小球肾炎的发展,该疾病的特征是免疫复合物原位形成(卡穆西等人,《免疫学杂志》1986年,136:2127 - 2135)。本研究的目的是确定氯丙嗪在其他以免疫复合物原位形成为特征的大鼠模型中是否具有类似作用。在用与植入肾小球的外源性抗原反应的抗体诱导的肾小球肾炎中,氯丙嗪预处理可防止“驼峰”形成以及渗出性和增殖性病变。同样,氯丙嗪可预防皮肤中的被动性反向阿瑟斯反应。相比之下,当这些病变已经形成时,该药物无效,并且也未能抑制具有增强自体期的肾毒性血清肾小球肾炎的暴发性病程。有人提出,氯丙嗪的抗炎作用归因于其阻断炎症细胞募集和炎症介质释放的能力。