PDF(Pubmed)
Abstract：
Heat-killed Lactiplantibacillus plantarum L-137 (HK L-137) has been suggested to enhance the intestinal barrier in obese mice, leading to improvement of metabolic abnormalities and adipose tissue inflammation, and in healthy humans with overweight, leading to improvement of systemic inflammation. However, its detailed mechanism of action has not been clarified. Therefore, this study investigated the effects of HK L-137 on the permeability of rat small intestinal epithelial IEC-6 cells, tight junction-related gene and protein expression and localization, and intracellular signaling pathways involved in barrier function. Treatment of IEC-6 cells with HK L-137 for 26 h significantly reduced the permeability to fluorescein isothiocyanate-dextran (FD-4). HK L-137 also increased gene and protein expression of zonula occludens-1 (ZO-1), an important tight junction protein, without affecting the localization. Furthermore, inhibition of the extracellular signal-regulated kinase (ERK)1/2 pathway in IEC-6 cells canceled the HK L-137-related reduction in permeability to FD-4. Phosphorylation of ERK in IEC-6 cells was induced 15 min after the addition of HK L-137. These results suggest that HK L-137 reduces intestinal permeability partly through activating the ERK pathway and increasing expression of the ZO-1 gene and protein. Enhancement of intestinal barrier function with HK L-137 might be effective in preventing and treating leaky gut, for which no specific therapeutic tool has been established.
摘要：
热灭活的植物乳杆菌L-137（HKL-137）已被认为可以增强肥胖小鼠的肠道屏障，导致代谢异常和脂肪组织炎症的改善，在超重的健康人类中，改善全身炎症。然而,其详细作用机制尚未明确。因此,本研究探讨了HKL-137对大鼠小肠上皮IEC-6细胞通透性的影响,紧密连接相关基因和蛋白质的表达和定位，和细胞内信号通路参与屏障功能。用HKL-137处理IEC-6细胞26小时显着降低了异硫氰酸荧光素-葡聚糖（FD-4）的通透性。HKL-137还增加了小带虫1（ZO-1）的基因和蛋白质表达，一种重要的紧密连接蛋白，而不影响本地化。此外，IEC-6细胞中细胞外信号调节激酶（ERK）1/2途径的抑制消除了HKL-137相关的FD-4通透性降低。添加HKL-137后15分钟诱导IEC-6细胞中ERK的磷酸化。这些结果表明，HKL-137部分通过激活ERK途径和增加ZO-1基因和蛋白质的表达来降低肠道通透性。HKL-137增强肠屏障功能可能有效预防和治疗肠漏，尚未建立特定的治疗工具。
