高渗盐水预处理对肝脏缺血再灌注大鼠血清肿瘤坏死因子-α和IL-10水平的影响

Effects of Hypertonic Saline Pretreatment on Levels of TNF-α and IL-10 in Hepatic Ischemia-reperfusion Injury Rats

目的探讨高渗盐水预处理对肝脏缺血再灌注大鼠血清肿瘤坏死因子-α(TNF-α)和IL-10水平的影响。方法将45只清洁健康雄性SD大鼠随机分为3组:假手术组(Sham组)、缺血再灌注组(IR组)和高渗盐水预处理组(HTS组),各15只。各组建立大鼠肝脏缺血再灌注模型(Pringle′s法),观察肝脏缺血30min再灌注1、6、24h后血清天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、乳酸脱氢酶(LDH)、TNF-α和IL-10水平,以及再灌注6h后肝组织病理学和超微结构改变。结果IR组和HTS组各时点血清AST、ALT、LDH、TNF-α、IL-10水平与Sham组比较,差别有统计学意义(P<0.01);且HTS组各时点血清AST、ALT、LDH、TNF-α、IL-10水平与IR组比较,差别有统计学意义(P<0.01)。HTS组肝组织病理学和肝细胞超微结构损害明显轻于IR组。结论高渗盐水预处理通过抑制TNF-α的产生、增强IL-10的表达水平来对肝脏缺血再灌注损伤产生保护作用。

Objective To explore the effect of hypertonic saline （HTS） pretreatment on levels of TNF -α and IL - 10 and its protective mechanism in rats with hepatic ischemia reperfusion injury （HIRI）. Methods Forty - five clean and healthy male SD rats were randomly divided into 3 groups： sham operation group （ sham group ）, ischemia reperfusion group （ IR group） and HTS group, 15 in each, HIRI rat models were established by Pringle＇s method in all groups to determine the levels of serum aspartate aminotransferase （AST）, alanine aminotransferase （ALT）, lactate dehydrogenase （LDH）, TNF -α and IL- 10, at 1, 6, 24 h after 30 - minute IR, and to observe the changes of liver histopathology （HP） and ultrastructure 6 h after IR. Results At 1, 6 and 24h after reperfusion, the serum levels of ALT, AST, LDH and TNF - α were significantly lower in HTS group than in lR group （P 〈0.01） （HTS group： 565.00±16.76, 855.52±49.17, 1514.55±48.81 and 39.86± 4. 18, respectively; IR group： 627. 30 ± 43.15, 1250. 38 ± 55.29, 4251.53 ± 103.83 and 70, 92 ± 6. 70, respectively ）, and IL - 10 were significantly higher in HTS group than in IR group （ P 〈 0. 01 ） （ 139. 56 ± 10. 49, 79. 93 ± 5.40, respectively）. Every detected goal had more marked levels 6 h after reperfusion. The pathological and ultra - structure changes of liver were significantly slighter in HTS group than in IR group. Conclusion Hypertonic saline pretreatment protects IR - induced liver injury by inhibiting TNF - α production and increasing IL - 10 expression.