Lee Jeong-Hun, Chung Kyung-Sook, Shin Ji-Sun, Jung Seang-Hwan, Lee Sangmin, Lee Myung-Ki, Hong Hee-Do, Rhee Young Kyoung, Lee Kyung-Tae
Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University, Seoul 02447, Korea.
Department of Biomedical and Pharmaceutical Sciences, Graduate School, Kyung Hee University, Seoul 02447, Korea.
Polymers (Basel). 2022 Aug 31;14(17):3594. doi: 10.3390/polym14173594.
We previously reported the immunostimulatory effect of an exopolysaccharide fraction from KFT18 (PE-EPS), a lactic acid bacterium, in macrophages and primary splenocytes, as well as in cyclophosphamide-induced immunosuppressed mice. In this study, the anti-colitic activity of PE-EPS was investigated in a dextran sulfate sodium (DSS)-induced colitis animal model. PE-EPS relieved DSS-induced colitis symptoms, such as stool blood, decreased colon length, crypt disruption, and mucus layer edema. Regarding the molecular mechanism, PE-EPS reduced the enhanced expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokines (TNF-α, IL-6, and IL-1) in the colon tissue of colitis-induced mice. Additionally, PE-EPS protected against DSS-induced phosphorylation of p65 and signal transducer and activator of transcription 1 (STAT1). These findings suggested that the exopolysaccharide fraction from KFT18 can be used to treat inflammatory bowel disease by alleviating colonic inflammation.
我们之前报道了来源于乳酸菌KFT18的胞外多糖组分(PE-EPS)在巨噬细胞和原代脾细胞中以及在环磷酰胺诱导的免疫抑制小鼠中的免疫刺激作用。在本研究中,我们在葡聚糖硫酸钠(DSS)诱导的结肠炎动物模型中研究了PE-EPS的抗结肠炎活性。PE-EPS缓解了DSS诱导的结肠炎症状,如便血、结肠长度缩短、隐窝破坏和黏液层水肿。关于分子机制,PE-EPS降低了结肠炎诱导小鼠结肠组织中诱导型一氧化氮合酶(iNOS)、环氧化酶-2(COX-2)和促炎细胞因子(TNF-α、IL-6和IL-1)的表达增强。此外,PE-EPS可防止DSS诱导的p65磷酸化以及信号转导和转录激活因子1(STAT1)的磷酸化。这些发现表明,来源于KFT18的胞外多糖组分可通过减轻结肠炎症来治疗炎症性肠病。