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江浙蝮蛇毒酸性磷脂酶Ａ２（ＡＰＬＡ２）对多种致聚剂引起的血小板聚集具有抑制作用，这种抑制并非是由于ＡＰＬＡ２与血小板膜结合，引起膜流动性降低造成。ＡＰＬＡ２不裂解血小板，电镜观察表明它能抑制血小板内部颗粒的中心化，使之不易被激活。进一步研究显示ＡＰＬＡ２是作用在细胞骨架上，使致聚剂引起的朋动蛋白单体聚合难以进行，ＡＰＬＡ２导致的ｃＡＭＰ浓度的升高正说明了这点。结果提示ＡＰＬＡ２首先作用于血小板细胞膜。引起ｃＡＭＰ浓度升高，影响到细胞骨架的正常功能，进而抑制了血小板的聚集。
Jiangsu and Zhejiang viper venom acid phospholipase A2 (APLA2) on a variety of polymerization inhibitor induced platelet aggregation inhibition, this inhibition is not due to APLA2 and platelet membrane binding, resulting in reduced membrane fluidity caused. APLA2 does not lyse platelets, electron microscopy showed that it can inhibit the central platelet particles, making it difficult to be activated. Further studies showed that APLA2 acts on the cytoskeleton, making it difficult to polymerize cofactor monomers due to the polymerization agent, as demonstrated by the increased cAMP concentration induced by APLA2. The results suggest that APLA2 first acts on the platelet membrane. Caused by increased cAMP concentration, affecting the normal function of the cytoskeleton, thereby inhibiting the aggregation of platelets.