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大鼠酵母聚糖性胸膜炎中细胞内和细胞外磷脂酶A2活性

Cellular and extracellular phospholipase A2 activity in zymosan pleurisy in rat.

作者信息

Morgan D W, Anderson C, Meyers K, Coffey J, Moody K, Welton A

机构信息

Department of Allergy and Inflammation, Hoffmann-LaRoche, Inc., Nutley, NJ 07110.

出版信息

Adv Exp Med Biol. 1990;275:145-54. doi: 10.1007/978-1-4684-5805-3_9.

Abstract

The pleural exudate from rats treated intrapleurally with zymosan contains phospholipase A2 (PLA2) activity which is Ca2(+)-independent and optimally active at a neutral pH. This PLA2 activity was found in approximately equal amounts in both the cellular and extracellular fractions of the exudate. The Ca2(+)-independency of the PLA2's in the pleural exudate distinguishes them from plasma PLA2's and this suggests that the source of the exudate PLA2's is not plasma. The appearance of PLA2 activity in zymosan-induced pleural exudate correlates temporally with increases in exudate volume and pleural cell number. In all cases, the maximum response was seen 24 hr after zymosan challenge. All parameters of pleurisy and PLA2 activity are similarly sensitive to the steroid dexamethasone which has been hypothesized to act, in part, through the synthesis of PLA2 inhibitory peptides. In its entirety, this information suggests that there is a relationship between pleural PLA2 activity and the appearance of pleural inflammation (exudate volume and cells) and that PLA2 may play an important role in the initiation and propagation of this inflammatory process in rats. Furthermore, the zymosan-induced pleurisy model may serve as a useful model for the identification of PLA2 inhibitors with antiinflammatory activity.

摘要

经胸膜内注射酵母聚糖处理的大鼠的胸腔渗出液含有磷脂酶A2(PLA2)活性,该活性不依赖于Ca2+,在中性pH值下活性最佳。在渗出液的细胞和细胞外部分中发现的这种PLA2活性含量大致相等。胸腔渗出液中PLA2的Ca2+非依赖性使其与血浆PLA2区分开来,这表明渗出液PLA2的来源不是血浆。酵母聚糖诱导的胸腔渗出液中PLA2活性的出现与渗出液体积和胸膜细胞数量的增加在时间上相关。在所有情况下,酵母聚糖攻击后24小时出现最大反应。胸膜炎的所有参数和PLA2活性对类固醇地塞米松同样敏感,据推测地塞米松部分通过合成PLA2抑制肽起作用。总体而言,这些信息表明胸腔PLA2活性与胸膜炎症的出现(渗出液体积和细胞)之间存在关系,并且PLA2可能在大鼠这种炎症过程的起始和传播中起重要作用。此外,酵母聚糖诱导的胸膜炎模型可能作为鉴定具有抗炎活性的PLA2抑制剂的有用模型。

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