Cirino G, Cicala C, Sorrentino L
Department of Experimental Pharmacology, University of Naples Federico II, Italy.
Inflammation. 1994 Feb;18(1):59-66. doi: 10.1007/BF01534598.
In this study by using the human recombinant non-pancreatic-secreted platelet PLA2 (r-hnps-PLA2) and rabbit polyclonal antibodies directed against either the human (group II) or the porcine enzyme (group I), we have shown a possible involvement of platelet PLA2 in poly-L-arginine (25 kDa)-induced rat paw edema. Local treatment of rats with the anti-platelet-PLA2 antibody (anti-hnps-PLA2) but not with anti-porcine-PLA2 antibody (anti-porc-PLA2) significantly reduced the edema induced by a maximal dose of poly-L-arginine (1 mg/paw). Furthermore when r-hnps-PLA2 (1-10 micrograms) was injected together with a subliminal dose of poly-L-arginine (50 micrograms/paw), a dose-dependent increase in both edema and protein leakage was observed. This effect was selectively inhibited by the anti-hnps-PLA2 (10-100 micrograms/paw) but not anti-porc-PLA2 (10-100 micrograms paw). Thus, platelets seem to be involved in both vascular and cellular components of the inflammatory response by contributing, most likely in the early phase, to the edema formation through secretion of PLA2.
在本研究中，通过使用人重组非胰腺分泌型血小板磷脂酶A2（r-hnps-PLA2）以及针对人（II组）或猪酶（I组）的兔多克隆抗体，我们已表明血小板磷脂酶A2可能参与聚-L-精氨酸（25 kDa）诱导的大鼠爪肿胀。用抗血小板磷脂酶A2抗体（抗-hnps-PLA2）而非抗猪磷脂酶A2抗体（抗-porc-PLA2）对大鼠进行局部治疗，可显著减轻最大剂量聚-L-精氨酸（1 mg/爪）诱导的肿胀。此外，当r-hnps-PLA2（1 - 10微克）与阈下剂量的聚-L-精氨酸（50微克/爪）一起注射时，观察到肿胀和蛋白质渗漏均呈剂量依赖性增加。这种效应被抗-hnps-PLA2（10 - 100微克/爪）选择性抑制，而抗-porc-PLA2（10 - 100微克/爪）则无此作用。因此，血小板似乎通过在炎症反应的早期阶段极有可能通过分泌磷脂酶A2促进水肿形成，从而参与炎症反应的血管和细胞成分。
