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说明：
关键词： 腰椎间盘突出,磷脂酶A2（PLA2）
腰椎间盘突出引起腰痛和坐骨神经痛的原因还不清楚。脊神经根受压不是在所有情况下都与临床疼痛症状相关。椎间盘突出病人行化学髓核溶解术后坐骨神经疼痛症状减轻，但CT扫描显示机械压迫仍然存在，这提示脊神经根机械压迫能引起伤害但不一定引起疼痛〔1〕。大量临床研究证明，机械压迫不是引起神经根痛和功能障碍的唯一原因。Kuslish等〔2〕提示在行硬膜外麻醉或局麻摘除突出椎间盘的手术过程中，受压的神经根对机械刺激非常敏感。McCarron等〔3〕和Olmarker等〔4〕的动物实验表明，椎间盘髓核能引起硬膜、神经根袖和马尾神经的炎症表现。现在虽不能确定哪种成分或化学因子在椎间盘突出后的炎症反应中起主要作用，但近来大量的研究表明，磷脂酶A2（PLA2）在突出的椎间盘组织中呈非常高的活性，且从椎间盘组织中纯化的PLA2具有致炎特性。现对PLA2在椎间盘突出后的发病过程中的作用作一综述。
1 PLA2的分子生物学
PLA2（磷脂-2-酰基水解酶，EC3.1.1.4）是一个脂解酶，特异水解糖磷脂2位酰基部位，生成溶血磷脂和自由脂肪酸，主要是花生四烯酸，这是炎症级联反应的一个重要步骤。花生四烯酸被进一步转变为前列腺素和其它花生酸，如血栓素、白三烯、血小板活化因子，它们是炎症反应的强力介质。PLA2的生物学作用有如下几个方面：①通过酶解作用产生炎性介质；②酶解产物溶血磷脂和不饱和自由脂肪酸能直接破坏细胞膜并引起水肿；③PLA2的作用底物是细胞膜磷脂，因此PLA2可直接引起细胞膜损害；④PLA2能兴奋伤害感受器，引起疼痛〔5〕。
目录：
1 PLA2的分子生物学
2 退变椎间盘中PLA2活性升高
3 PLA2在椎间盘疾病中的作用机理
4 PLA2拮抗剂治疗椎间盘突出症
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