一氧化碳保护大鼠肠道对抗LPS的作用机制

目的： 探讨外源性CO对LPS攻击时大鼠肠道的保护作用及作用机制。 方法： 血气分析监测大鼠呼吸参数，在1、3、6 h的时点上，分别对空白组、脂多糖组（LPS，5 mg/kg）、低浓度CO吸入组（CO 250 mL/M3）、腹腔内CO注射组（CO 2 mL/kg）、脂多糖CO吸入组（LPS 5 mg/kg+CO 250 mL/M3）和脂多糖血症CO腹腔内注射组（LPS 5 mg/kg+CO 2 mL/kg），用硫代巴比妥酸法（TBA）测定肠道丙二醛（MDA）含量，用羟胺法测定超氧化物歧化酶（SOD）活性，并应用RT-PCR检测肠道组织内的血红素氧合酶-1（HO-1）mRNA的变化。 结果: 给予250 mL/M3的CO持续吸入以及2 mL/kg的CO腹腔内注射，在1、3、6 h时点上，大鼠无缺氧情况的出现。两种方法给予外源性的CO，均降低了内毒素血症时大鼠肠道组织中的MDA含量，提高了SOD的活性，同时诱导了肠组织的HO-1 mRNA 的表达。 结论: 低浓度的CO吸入（250 mL/M3）和一次性腹腔内注射CO（2 mL/kg）补充对大鼠是安全的，补充低浓度或小剂量的外源性CO可以对脂多糖血症肠道提供保护作用，并可以刺激HO-1的产生，促进内源性的CO产生发挥抗炎作用。

Mechanism of carbon monoxide protects rat intestine against LPS

AIM:To study the effect of exogenous carbon monoxide on rat intestine attacked by LPS.METHODS:The experimental rats were divided into 6 groups randomly:normal group,lipopolysaccharide(LPS,5 mg/kg) group,CO inhalation(250 mL/M3) group,CO intraperitoneal injection(2 mL/kg) group,LPS(LPS 5 mg/kg) with CO inhalation(250 mL/M3) group and LPS(LPS 5 mg/kg) with CO intraperitoneal injection(2 mL/kg) group.The PaO2,PaCO2,SO2 and COHb were monitored.Rat intestine malondialdehyde(MDA) with thiobarbitric acid(TBA) and superoxide dismutase(SOD) with hydroxylamine were detected and heme oxygenase-1(HO-1) mRNA expression were checked by RT-PCR.RESULTS:Low concentration of CO inhalation(250 mL/M3) and CO intraperitoneal injection(2 mL/kg) did not cause the rat hypoxia.Compared to control group,exposure exogenous CO,the MDA content in LPS attacked rat intestine decreased,the SOD activity and the expression of HO-1 mRNA increased.CONCLUSIONS:Low concentration of CO inhalation(250 mL/M3) and low dose CO intraperitoneal injection(2 mL/kg) are safe to rat.Exposure exogenous CO protects rat intestine against LPS attack,CO induces the HO-1 mRNA expression and exerts anti-inflammation via endogenous CO.