颈交感神经阻滞调节放烧复合伤小鼠巨噬细胞GR的表达及细胞因子分泌的影响

Effects of cervical sympathetic ganglia block on GR expression and cytokine release of macrophage in mice with combined radiation and burn injury

目的探讨颈交感神经阻滞(cervical sympathetic ganglia block,SB)在放烧复合伤小鼠腹腔巨噬细胞糖皮质激素受体(glucocorticoid receptor,GR)表达及炎性细胞因子分泌中的作用。方法TBSA15%Ⅲ度烧伤合并5Gy放射损伤小鼠分为单纯放烧复合伤组、放烧复合伤后单侧颈部SB治疗组、放烧复合伤后双侧颈部SB治疗组,另设正常对照组,每组8只,比较各组巨噬细胞GR水平及巨噬细胞分泌炎性细胞因子TNF-α、IL-1β、IL-6的差异。结果单侧及双侧SB组腹腔巨噬细胞GR蛋白水平均显著高于放烧复合伤组(P<0.01),单侧及双侧SB组腹腔巨噬细胞分泌TNF-α、IL-1β、IL-6的作用均显著低于放烧复合伤组(P<0.05)。放烧复合伤后颈部单侧SB组与双侧SB组间巨噬细胞GR蛋白水平及TNF-α、IL-1β、IL-6的表达释放无明显差异(P>0.05)。结论单侧或双侧颈部SB均可改善放烧复合伤巨噬细胞GR功能,抑制其过度分泌炎性细胞因子。

Objective To explore the roles of cervical sympathetic ganglia block （SB） in glucocorticoid receptor（GR） , protein levels and proinflammatory cytokine release of peritoneal macrophage in mice with combined radiation and burn injury. Methods Thirty-two Kunming mice were divided into control group, injury group （ inflicted with 5 Gy irradiation and 15% TBSA full thickness burn injury）, unilateral SB （ inflicted with injury, treated daily by unilateral cervical SB） and bilateral SB group （ inflicted with injury, treated daily by bilateral cervical SB）. The roles of SB were evaluated by comparing GR protein levels and proinflammatory cyto-kine （ TNF-α, IL-1β, IL-6） release of peritoneal macrophage in each group. Results Compared with control group, GR protein levels in injury group decreased significantly. The levels of unilateral SB and bilateral SB group were lower than that of control group but higher than that of injury group. Proinflammatory cytokine （TNF-α, IL-1β, IL-6） release in unilateral SB and bilateral SB groups was higher than that in control group but significantly lower than injury group. There were no significant differences of GR protein levels and proinflammatory cytokine （TNF-α, IL-1β, IL-6 ） release between unilateral SB and bilateral SB groups. Conclusion Bilateral SB and unilateral SB can be an effective therapeutic approach for ameliorating GR function and controlling inflammatory response of peritoneal macrophage following severe trauma.