L-茶氨酸对产肠毒素大肠杆菌引起的免疫应激小鼠肠道的保护作用研究

Study on the Protective Effect of L-Theanine on the Intestinal in Mice with Immune Stress Induced by ETEC

以SPF级Balb/c雌性小鼠为实验动物,对其适应性饲养3 d后连续30 d灌喂不同剂量L-茶氨酸,然后腹腔注射产肠毒素大肠杆菌E44813诱导免疫应激,5 h后取样,分析研究了L-茶氨酸对小鼠体重,回肠组织谷胱甘肽过氧化物酶(Glutathione peroxidase,GSH-Px)、过氧化氢酶(Homogenate catalase,CAT)与诱导型一氧化氮合成酶(Inducible nitric oxide synthase,i NOS)活性,丙二醛(Malondialdehyde,MDA)含量、空肠组织病理学变化,以及血清肿瘤坏死因子α(Tumor necrosis factor-α,TNF-α)、细胞间粘附分子1(Intercellular cell adhesion molecule-1,ICAM-1)和白介素1β(Interleukin-1β,IL^(-1)β)表达量的影响,以探明L-茶氨酸对产肠毒素大肠杆菌免疫应激小鼠肠道的保护作用。结果表明,各剂量L-茶氨酸均能显著增加小鼠体重,可减轻产肠毒素大肠杆菌E44813引起的肠道组织病变程度,升高回肠组织GSH-Px和CAT酶活性,降低MDA含量和i NOS酶活性,在不同程度上抑制血清TNF-α、IL^(-1)β和ICAM-1的表达量。说明L-茶氨酸可通过抑制炎性细胞因子表达水平、降低脂质过氧化程度和提高抗氧化能力来维护肠道组织形态与结构的完整性,并达到保护肠道的作用。

SPF grade Balb/c female mice were used as experimental animals. After adaptive feeding for 3 days, mice were orally pre-treated with different dosages of L-theanine once daily for 30 days before ETEC E44813 intraperitoneal injection. The body weight change in mice was analyzed during the breeding process. Mice were scarified 5 hours after ETEC injection and tissues were collected for analysis. The activities of ileum Glutathione peroxidase （GSH-Px）, homogenate Catalase （CAT）, Malondialdehyde （MDA） and Inducible nitric oxide synthase （iNOS） were measured and the pathological changes of intestinal and the levels of serum Tumor necrosis factor-α （TNF-α）, Interleukin-1β （IL-1β） and Intercellular cell adhesion molecule-1（ICAM-1） were examined. This study was aimed to explore the protective effects of L-theanine on intestinal of ETEC-induced immune stress model in mice. The results showed that： pretreatment with L-theanine at different dosages significantly increased mouse body weight; lowered the levels of ileum homogenate MDA and iNOS, improved the activities of ileum homogenate CAT, GSH-Px, decreased the expressions of serum TNF-α、 IL-1β and ICAM-1, and improved pathological structure of jejunum tissue. These data demonstrated that pre-treatment with L-theanine prevented ETEC-induced intestinal injury through inhibiting TNF-α、 IL-1β and ICAM-1, and inflammatory reaction and enhancing intestinal antioxidant abilities.