为探讨丙泊酚对葡聚糖硫酸钠(dextran sodium sulfate, DSS)诱导的结肠炎小鼠病理损伤和免疫反应的影响，构建DSS诱导的结肠炎小鼠模型，将小鼠随机分为5组：对照组、模型组、丙泊酚低剂量组、丙泊酚中剂量组和丙泊酚高剂量组。采用疾病活动指数评分检测小鼠体质量变化和结肠长度，H-E染色检测病理损伤程度并进行组织病理学评分，末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（terminal dexynucleotidyl transferase-mediated dUTP nick-end labeling，TUNEL）染色检测细胞凋亡情况，qRT-PCR检测IL-1β、IL-6、TNF-α、IL-10 mRNA水平，ELISA检测IL-1β、IL-6、TNF-α、IL-10水平，Western blotting检测p65、p-p65蛋白表达。结果显示，与对照组比较，模型组小鼠体质量显著降低（P＜0.05），结肠长度显著缩短（P＜0.05），病理学评分显著升高（P＜0.05），结肠细胞凋亡率显著增加（P＜0.05），IL-1β、IL-6、TNF-α mRNA水平显著升高（P＜0.05），IL-10 mRNA水平显著降低（P＜0.05），IL-1β、IL-6、TNF-α水平显著升高（P＜0.05），p-p65/p65比值显著升高（P＜0.05）；与模型组比较，丙泊酚中、高剂量组小鼠体质量显著升高（P＜0.05），结肠长度显著增加（P＜0.05），病理学评分显著降低（P＜0.05），结肠细胞凋亡率显著降低（P＜0.05），IL-1β、IL-6、TNF-α mRNA水平显著降低（P＜0.05），IL-10 mRNA水平显著升高（P＜0.05），IL-1β、IL-6、TNF-α水平显著降低（P＜0.05），IL-10水平显著升高（P＜0.05），p-p65/p65比值显著降低（P＜0.05）。该研究提示，丙泊酚通过抑制NF-κB p65的磷酸化缓解DSS诱导的结肠炎小鼠病理损伤和免疫反应。

To investigate the effects of propofol on pathological injury and immune response in mice with colitis induced by dextran sodium sulfate(DSS), mice were randomly divided into 5 groups: the control group, the model group, the low-dose propofol group, the medium-dose propofol group and the high-dose propofol group. The changes of body weight and colon length were measured by disease activity index score; the pathological injury degree and histopathological score were detected by H-E staining; apoptosis was detected by treminal dexynucleotidyl transferase-mediated dUTP nick-end labeling（TUNEL） staining; the mRNA levels of IL-1β, IL-6, TNF-α and IL-10 were measured by qRT-PCR; the levels of IL-1β, IL-6, TNF-α and IL-10 were measured by ELISA, and the protein expressions of p65 and p-p65 were detected by Western blotting. The results showed that compared with the control group, the body weight of the model group significantly reduced（P＜0.05）, colon length decreased significantly（P＜0.05）, pathology score significantly higher（P＜0.05）, the apoptosis rate increased significantly（P＜0.05）, IL-1β, IL-6, TNF-α mRNA levels were significantly increased（P＜0.05）, IL-10 mRNA level was significantly lower（P＜0.05）, IL-1β, IL-6, TNF-α expressions significantly increased（P＜0.05）, and the p-p65/p65 ratio increased significantly（P＜0.05）. Compared with the model group, the body weight of the propofol middle- and high-dose groups significantly increased（P＜0.05）, as well as the length of the colon（P＜0.05）, pathology score decreased significantly （P＜0.05）, the apoptosis rate was significantly lower（P＜0.05）, IL-1β, IL-6, TNF-α mRNA levels decreased significantly（P＜0.05）, IL-10 mRNA level increased significantly（P＜0.05）, IL-1β, IL-6, TNF-α expressions decreased significantly（P＜0.05）, IL-10 content increased significantly（P＜0.05）, the p-p65 /p65 ratio was significantly reduced（P＜0.05）.The study suggests that propofol could alleviate the pathological injury and immune response of mice with colitis induced by DSS via inhibiting the phosphorylation of NF-κB p65.