CAJ | 학술논문

目的：探讨Th1/Th2细胞因子IL-2，干扰素-γ(interferon-γ，IFN-γ)，IL-4和IL-10在葡聚糖酸钠(dextran sulfate sodium，DSS)诱导的大鼠实验性溃疡性结肠炎治疗模型中的表达。方法：雄性Sprague Dawley 大鼠40只，随机均分为正常组、模型组、柳氮磺嘧啶治疗组(SASP组)、结肠宁治疗组(结肠宁组)，每组各10只。对各组大鼠进行疾病活动指数评分(disease activity index，DAI)及结直肠组织损伤学评分，运用酶联免疫吸附测定(enzyme-linked immunosorbent assay，ELISA)及real-time PCR检测血清及肠黏膜组织中细胞因子IL-2，IFN-γ，IL-4和IL-10含量水平。结果：与模型组比较，结肠宁组大鼠的DAI及结直肠组织损伤学评分均明显下降(均P<0.05)；但与SASP组比较，差异无统计学意义(P>0.05)。血清和组织中IL-2表达在治疗前后的各组间比较，差异均无统计学意义(均P>0.05)。SASP组和结肠宁组血清及肠黏膜组织IFN-γ水平较模型组下调，血清中差异均有统计学意义(均P<0.05)，肠黏膜组织中仅结肠宁组差异均有统计学意义(均P<0.05)。SASP组和结肠宁组血清IL-4水平较模型组均上调，但只有结肠宁组差异有统计学意义(P<0.05)；而肠黏膜组织中差异均无统计学意义(均P>0.05)。SASP组和结肠宁组血清及肠黏膜组织IL-10水平较模型组上升，差异均有统计学意义(均P<0.05)。SASP组和结肠宁组血清及肠黏膜组织中细胞因子IL-2，IFN-γ，IL-4和IL-10含量水平比较，差异均无统计学意义(均P>0.05)。结论：DSS造模破坏Th1/Th2在结肠中的表达平衡。结肠宁能改善DSS所致的实验性溃结大鼠模型炎症，通过上调血清和肠黏膜组织IL-10水平、下调IFN-γ水平可保持Th1/Th2细胞间平衡，从而改善免疫功能。
목적：탐토Th1/Th2세포인자IL-2，간우소-γ(interferon-γ，IFN-γ)，IL-4화IL-10재포취당산납(dextran sulfate sodium，DSS)유도적대서실험성궤양성결장염치료모형중적표체。방법：웅성Sprague Dawley 대서40지，수궤균분위정상조、모형조、류담광밀정치료조(SASP조)、결장저치료조(결장저조)，매조각10지。대각조대서진행질병활동지수평분(disease activity index，DAI)급결직장조직손상학평분，운용매련면역흡부측정(enzyme-linked immunosorbent assay，ELISA)급real-time PCR검측혈청급장점막조직중세포인자IL-2，IFN-γ，IL-4화IL-10함량수평。결과：여모형조비교，결장저조대서적DAI급결직장조직손상학평분균명현하강(균P<0.05)；단여SASP조비교，차이무통계학의의(P>0.05)。혈청화조직중IL-2표체재치료전후적각조간비교，차이균무통계학의의(균P>0.05)。SASP조화결장저조혈청급장점막조직IFN-γ수평교모형조하조，혈청중차이균유통계학의의(균P<0.05)，장점막조직중부결장저조차이균유통계학의의(균P<0.05)。SASP조화결장저조혈청IL-4수평교모형조균상조，단지유결장저조차이유통계학의의(P<0.05)；이장점막조직중차이균무통계학의의(균P>0.05)。SASP조화결장저조혈청급장점막조직IL-10수평교모형조상승，차이균유통계학의의(균P<0.05)。SASP조화결장저조혈청급장점막조직중세포인자IL-2，IFN-γ，IL-4화IL-10함량수평비교，차이균무통계학의의(균P>0.05)。결론：DSS조모파배Th1/Th2재결장중적표체평형。결장저능개선DSS소치적실험성궤결대서모형염증，통과상조혈청화장점막조직IL-10수평、하조IFN-γ수평가보지Th1/Th2세포간평형，종이개선면역공능。
Objective: To investigate the expression of Th1/Th2 inflammatory cytokines IL-2, interferon-γ (IFN-γ), IL-4, and IL-10 in rat treatment model of dextran sulfate sodium (DSS) -induced ulcerative colitis. Methods: Forty Sprague Dawley (SD) male rats were divided into a normal group, a colitis model group, a sulfasalazine(SASP)-treatment group (SASP group) and a Jiechangning-treatment group (Jiechangning group) (each groupn=10). Disease activity index (DAI) and colorectal histological damage scale were assessed. The expression levels of cytokines IL-2, IFN-γ, IL-4, and IL-10 in the serum and the colon mucosa tissues were detected by enzyme-linked immuno sorbent assay (ELISA) and real time polymerase chain reaction (RT-PCR). <br> Results: Compared with the colitis model group, the DAI and colorectal histological damage scale were decreased in the Jiechangning group (bothP<0.05), but there was no obvious difference compared with the SASP group (P>0.05). There was no signiifcant difference in IL-2 expression both in the serum and the colon mucosa tissues before or after the treatment in various groups (P>0.05). Compared with the colitis model group, IFN-γ level both in the serum and the colon mucosa tissues was decreased in the SASP group and the Jiechangning group, with significant difference in the serum (bothP<0.05), but there was significant difference in the colon mucosa tissues only in the Jiechangning group (P<0.05). The serum IL-4 level in the SASP group and the Jiechangning group was increased compared with that in the colitis control group, with significant difference only in the Jiechangning group (P<0.05). There was no difference in IL-4 level in the colon mucosa tissues whether treated or not (P>0.05). IL-10 level both in the serum and the colon mucosa tissues in the SASP group and the Jiechangning group was increased compared with that in the colitis model group, with significant difference (allP<0.05). There was no difference in the expression level of cytokines IL-2, IFN-γ, IL-4, and IL-10 both in the serum and the colon mucosa tissues between the SASP group and the Jiechangning group (allP>0.05). <br> Conclusion: DSS can break the balance of Th1/Th2 expression in the colon. Jiechangning enema can ameliorate DSS-induced acute experimental colitis in rats by decreasing IFN-γ level and increasing IL-10 level both in the serum and the colon mucosa tissues to regulate the Th1/Th2 balance and improve immunity.