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本研究观察了闭合性创伤小鼠Ｔ细胞膜流动性的变化及其与Ｔ细胞功能之间的关系。结果显示，创伤后Ｔ细胞质膜、线粒体膜、微粒体膜流动性均降低，且这一变化同创伤后Ｔ淋巴细胞转化降低、白细胞介素２（ＩＬ－２）产生减少，ＩＬ－２受体（ＩＬ－２Ｒ）表达受抑、ＩＬ－２介导的淋巴细胞增殖反应低下显著相关。创伤后Ｔ细胞内丙二醛（ＭＤＡ）含量增高。维生素Ｅ（ＶＥ）和超氧化物歧化酶（ＳＯＤ）体内应用可明显降低创伤小鼠Ｔ细胞内ＭＤＡ含量、提高Ｔ细胞膜的流动性，并可逆转Ｔ细胞功能的受抑状态。表明创伤后脂质过氧化反应可降低Ｔ细胞膜的流动性，进而导致Ｔ细胞功能受抑。
This study investigated the changes of T cell membrane fluidity and its relationship with T cell function in closed traumatized mice. The results showed that the fluidity of plasma membrane, mitochondrial membrane and microsomal membrane of T cells decreased after trauma, and this change was associated with the decrease of T lymphocyte transformation, the decrease of interleukin 2 (IL-2) production and the decrease of IL-2 receptor (IL-2R) expression was suppressed, IL-2-mediated lymphocyte proliferation was significantly correlated. Posttraumatic T cells increased the content of malondialdehyde (MDA). Vitamin E (VE) and superoxide dismutase (SOD) in vivo can significantly reduce the T cell MDA content in trauma mice, improve the mobility of T cell membrane, and can reverse the suppression of T cell function. That post-traumatic lipid peroxidation can reduce the mobility of T cell membrane, leading to T cell dysfunction.