This study aimed to evaluate the effects of intestinal damage repair of epidermal growth factor (EGF) on dextra sulfate sodium (DSS)-induced colitis in mice.Twenty-four BALB/C mice aged at 6 weeks were randomly assigned into three groups:normal control group,DSS model control group and DSS+EGF group.The normal control group received normal drinking water;DSS model control group received 5％ DSS solution in drinking water for 7 consecutive days and followed with normal drinking water for 3 days;DSS + EGF group received the same treatment of DSS as DSS model control group,meanwhile,these mice were administered with EGF by intraperitoneal injection twice a day and for 10 days.The results showed as follows:1) DSS model control group significantly shortened colon length of mice compared with the normal control group (P＜0.01),and DSS+EGF group significantly increased colon length of mice compared with the DSS model control group (P＜0.01).2) Mice in DSS model control group revealed a typical ulcer of the colonic tissues,and significant increased colonic damage score (CDS) compared with the normal control group (P＜ 0.01).Mice in DSS+EGF group did not show the ulcer of the colonic tissues,and significantly reduced CDS compared with DSS model control group (P＜0.01).3) DSS model control group significantly decreased colonic tight junction proteins (Occludin) concentration of mice compared with normal control group (P＜0.05).DSS+EGF group significantly increased colonic Occludin concentration of mice compared with DSS model control group (P＜0.05).4) DSS model control group significantly decreased colonic interleukin (IL)-2 (P＜ 0.01),IL-4 (P＜0.01) and IL-10 concentrations (P ＜ 0.05) of mice compared with normal control group.DSS+EGF group significantly increased colonic IL-2 (P＜0.01),IL-4 (P＜ 0.01) and IL-10 concentrations (P＜0.05) of mice compared with DSS model control group.The results show that EGF can repair damaged intestinal tissue and maintain the integrity of the intestinal mucosal barrier by increasing intestinal Occludin expression and regulation of levels of intestinal cytokines concentrations.%本文旨在讨论表皮生长因子(EGF)对葡聚糖硫酸钠(DSS)诱导的结肠炎模型小鼠肠道损伤的修复作用.选用24只6周龄BALB/c小鼠,随机分为3组,即:正常对照组、DSS模型对照组、DSS+EGF组.正常对照组小鼠饮用自来水;DSS模型对照组小鼠在试验第1～7天饮用5％DSS水溶液,第8～10天饮用自来水;DSS+EGF组小鼠按照DSS模型对照组处理,同时每天皮下注射EGF2次,共注射10 d.结果表明:1)与正常对照组相比,DSS模型对照组小鼠结肠长度极显著降低(P＜0.01);与DSS模型对照组相比,DSS+EGF组小鼠结肠长度极显著增加(P＜0.01).2)DSS模型对照组小鼠结肠可见典型溃疡,结肠损伤程度评分(CDS)极显著高于正常对照组(P＜0.01);DSS+EGF组小鼠结肠组织未见溃疡,与DSS模型对照组相比,CDS极显著降低(P＜0.01).3)与正常对照组相比,DSS模型对照组小鼠结肠紧密连接蛋白(Occludin)浓度显著降低(P＜0.05);与DSS模型对照组相比,DSS+EGF组小鼠结肠Occludin浓度显著升高(P＞0.05).4)与正常对照组相比,DSS模型对照组小鼠结肠白细胞介素-2(IL-2)和白细胞介素-4(IL-4)浓度极显著降低(P＜0.01),白细胞介素-10(IL-10)浓度显著降低(P＜0.05);与DSS模型对照组相比,DSS+EGF组结肠IL-2和IL-4浓度极显著增加(P＜0.01),IL-10浓度显著增加(P＜0.05).由此可见,EGF可能通过提高肠道Occludin表达水平,调节肠道细胞因子浓度趋于正常水平,从而修复受损肠道组织,维持肠道黏膜屏障的完整性.
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