摘要
研究了创伤小鼠活化T细胞内cAMP代谢、蛋白激酶A(PKA)活性的变化及同T细胞功能的关系。结果显示,创伤后活化T细胞内cAMP含量增加,这一变化同创伤后T细胞白介素2(IL-2)生成减少,IL-2受体(IL-2R)表达受抑,T淋巴细胞转化(TLT)降低密切相关。创伤后活化T细胞内腺苷酸环化酶(AC)、PKA活性增加,cAMP-磷酸二酯酶(cAMP-PDE)活性降低。PKA抑制剂H-8在体外可明显逆转创伤小鼠T细胞功能的受抑状态。提示cAMP-PKA途径参与了创伤后T细胞功能的抑制过程。AC活性增加、cAMP-PDE活性降低是导致T细胞内cAMP含量增加的原因。
he changes of cAMP metabolism ,protein kinaseA(PKA)activity
in activated T cells andtheir relationship with T cells functions were studied in traumatized
mice. The results showedthat the contents of cAMP in activated T cells were increased after
trauma,and this change wasclosely related to reduced interleukin 2(IL-2)preduction, suppressed
IL-2 receptor(IL-2R)ex-pression, decreased TIymphocytes transformation(TLT ) in T cells post
trauma. Adenylate cy-clase(AC )and PKA activity in activated T cells were increased after trauma
, while cAMP-phos-phediesterase(cAMP-PDE)activity was decreased.H 8,an inhibitor of PKA ,
can in vitro re-verse significantly suppressed T cells functions in traumatized mice . It is
suggested that cAMP-PKA pathway participates in suppressive process of T cells functions after
trauma. Increased ACactivity and decreased cAMP-PDE activity are causes resulting in elevated
content of cAMP in Tcells.
出处
《基础医学与临床》
CSCD
1995年第4期38-41,共4页
Basic and Clinical Medicine
基金
国家自然科学基金