烫伤大鼠腹腔巨噬细胞释放细胞因子作用的研究

ROLE OF MACROPHAGES IN RELEASING INFLAMMATION CYTOKINES IN SCALDED RATS

研究严重烫伤大鼠腹腔巨噬细胞释放TNF-α、IL-1β、IL-10等细胞因子的作用。通过建立烫伤动物模型,使用ELISA检测烫伤大鼠血浆TNF-α、IL-1β、IL-10的水平;收集烫伤大鼠及未烫伤大鼠的腹腔巨噬细胞,分别加入LPS(脂多糖)、LPS+DEX(地塞米松)共孵育;使用ELISA检测上清液中TNFα、IL-1β、IL-10的水平,比较两组大鼠间的差异。烫伤大鼠血浆出现高水平的TNFα-、IL-1β、IL-10;接受LPS刺激后,烫伤大鼠腹腔巨噬细胞分泌的TNFα-、IL-1β和IL-10的水平明显高于对照组。DEX对烫伤组大鼠腹腔巨噬细胞分泌细胞因子的抑制减少量显著低于对照组。由研究可知严重烫伤大鼠腹腔巨噬细胞释放的细胞因子与高细胞因子血症形成密切相关;烫伤可抑制巨噬细胞对DEX的反应性。

To investigate the roles of macrophages in releasing TNFα, IL-1βand IL-10 in heavy-degree scalded rats. Using enzyme-linked immunosorbent assay （ELISA）, we detected plasma TNF-α,IL-1βand IL-10 levels in heavy-degree scalded rats and sham rats. Peritoneal macrophages of scalded rats and sham rats were isolated and incubated with LPS, LPS ＋ DEX （dexamethosane） respectively; and their culture supernatants were detected for TNF-α, IL-βand IL-10 respectively. Plasma TNF-α, IL-βand IL-10 levels were significantly increased in heavydegree scalded rats, compared with sham rats. LPS could stimulate peritoneal macrophages of rats to release TNF- α,IL-1β and IL-10, and there were no significance between scalded rats and sham rats. LPS ＋ DEX could make the levels of TNF-α, IL-1βand IL-10 levels decrease in both groups, and the subtractions by inhibition of DEX in scalded rats were smaller than that in sham group. Activation of macrophages might play an important role in causing hypercytokinemia in scalded rats. The sensitivity of peritoneal macrophages to DEX might be inhibited in scalded rats.