摘要
采用 TBSA10%Ⅲ度烧伤小鼠模型探讨了烧伤后小鼠活化 T 细胞内游离钙浓度([Ca^(2+)]i)蛋白激酶 C(PKC)活性的变化及其同 T 细胞功能之间的关系。结果显示,烧伤后活化 T 细胞内[Ca^(2+)i]降低,PKC 活性下降,且这一变化同烧伤小鼠 T 细胞白介素2(IL-2)mRNA、IL-2受体α(IL-2Rα)mRNA 水平降低,IL-2生成减少,IL-2Rα表达受抑,T 淋巴细胞转化降低密切相关。钙离子导入剂A23187及 PKC 激活剂 TPA 在体外可分别提高烧伤小鼠活化 T 细胞内[Ca^(2+)]i、PKC 活性至正常对照水平,也可明显提高烧伤小鼠 T 细胞 IL-2及 IL-2Rα的基因表达水平,但不能使之恢复正常。提示活化T 细胞内[Ca^(2+)]i、PKC 活性降低是导致烧伤后 T 细胞功能受抑的原因之一。
TBSA 10%Ⅲ° burn mice model was used.The changes in free calcium concentration([Ca^(2+)]i)and protein kinase C(PKC)activity in activated T cells from burn mice,and their relationship with T cell functions was studied.The results showed that[Ca^(2+)]i and PKC activity in activated T cells were reduced after burn and these changes were closely related to reduced interleukin 2(IL-2)mRNA and IL-2 receptor α (IL-2Rα)mRNA levels,decreased IL-2 production,suppressed IL-2Rα expression,re- duced T lymphocytes transformation in T cells of burn mice.Calcium cation ionophore A 23187 and PKC activator TPA could in vitro elevate respectively[Ca^(2+)]i and PKC ac- tivity in activited T cells of burn mice.They also increased significantly IL-2 and IL-2Rα gene expression in T cells of burn mice,but not up to the normal control.It is suggested that reduced[Ca^(2+)]i,PKC activity in activated T cells may be one of the causes which produce suppression of T cell functions after burns.
基金
国家自然科学基金
