高盐饮食对内毒素休克小鼠IL-6 IL-12p40表达的影响

Effects of high salt on the expression of IL-6 and IL-12p40 in endotoxic shock mice

目的观察高盐饮食对小鼠内毒素休克致死率及炎症因子IL-6和IL-12p40表达的影响。方法雌性C57BL/6小鼠,6~8周,随机分为2组,每组各10只,高盐饮食组饮用含2.5%NaCl盐水;正常饮食组饮用不含NaCl的清水,喂食14d。腹腔注射脂多糖(LPS,500μg/只),观察小鼠的死亡率;腹腔注射LPS(200μg/只),观察小鼠血清、脾脏和腹腔细胞中细胞因子IL-6和IL-12p40水平。结果 1)高盐饮食组小鼠死亡率明显高于正常饮食组;2)与正常饮食组相比,高盐饮食组血清中IL-6和IL-12p40含量明显升高,差异具有统计学意义(t=5.534,P<0.01;t=2.906,P<0.05);3)与正常饮食组相比,高盐饮食组脾脏细胞中IL-6和IL-12p40 mRNA水平明显升高,差异具有统计学意义(t=4.075,P<0.05;t=4.758,P<0.01),腹腔细胞中IL-6和IL-12p40mRNA水平明显升高,差异具有统计学意义(t=25.47,P<0.001;t=8.589,P<0.001)。结论高盐饮食可增加内毒素休克小鼠的死亡率及其炎症因子IL-6和IL-12p40的分泌。

Objective To observe the effect of high salt on mortality of endotoxic shock mice and the ex- pression of inflammatory factors IL-6 and IL-12p40. Methods Twenty female mice were randomly divided into normal control group and high salt diets group. Respectively, the high salt group was fed with drink contai- ning 2.5 % NaCl and the normal control group was given water without NaCI. After 14 days, each mice was injected 500 wg LPS to observe mortality. And each mice was injected 200 btg LPS to observe the expression of IL-6 and IL-121M0 in serum,spleen and peritoneal cell Results 1 ） The mortality of high salt diet mice was obviously higher than normal diet group. 2 ） Compared with normal control group, the serum IL-5 and IL- 12p40 were significantly increased in high salt diet mice,and tile difference was statistically significant （ t = 5. 534 ,P 〈 0.01;t = 2.906 ,P 〈 0.05 ）. 3 ） Compared with normal control group, the expression of 1I,-6 and IL- 121o40 in spleen was significantly increased in high salt diet group,and the difference was statistically signifi- cant （ t = 4.075 ,P 〈 0.05 ; t = 4.758 ,P 〈 0.01 ）, The expression of IL-6 and IL-12p40 in peritoneal cells was sig- nificantiy increased in high salt diet group, and the difference was statistically significant （ t = 25.47, P 〈 0. 001 ; t = 8.589 ,P 〈 0.001 ）. Conclusion High salt diet increased the mortality of endotoxic shock mice and in- creased the secretion of inflammatory cytokines IL-6 and IL-12p40.