OBJECTIVE: To elucidate the recovery effect of LBS L on damaged intestinal epithelium and its miRNA-related mechanism.
METHODS: IEC-6 cells were used in vitro to assess the therapeutic effect of LBS L on the injured intestine and the regulation of miR-195-3p. Spermidine (SPD) with intestinal mucosal repair effect was used as a positive control. Sprague Dawley (SD) rats were subjected to 48 h fasting to induce intestinal epithelial atrophy in vivo. To determine the therapeutic effect of LBS L on injured intestinal epithelium and explore the mechanism, the fasting model group rats were treated with LBS L (25 mg/kg) for 4 days.
RESULTS: Results in vitro showed that LBS L (10 μM) promoted cell proliferation and migration, affecting the S phase of the cell cycle. Western blot signals showed that LBS L raised the expression level of occludin. The miR-195-3p levels were decreased following LBS L treatment, which could be inversed by transfecting miR-195-3p mimic, demonstrating that LBS L inhibited miR-195-3p to improve cell growth. Results in vivo showed that LBS L could reverse the atrophic villi and inflammatory cell infiltration in the submucosa and restore miR-195-3p, occludin, and Ki67 levels in the intestine of mice in the fasting group.
CONCLUSIONS: LBS L restores injured intestinal epithelium by reducing the expression of miR-195-3p.
目的:阐明LBSL对受损肠上皮的修复作用及其miRNA相关机制。
方法:在体外使用IEC-6细胞来评估LBSL对受损肠的治疗效果和miR-195-3p的调节。使用具有肠粘膜修复作用的亚精胺(SPD)作为阳性对照。SpragueDawley(SD)大鼠禁食48h,以诱导体内肠上皮萎缩。探讨LBSL对肠上皮损伤的治疗作用及其机制。禁食模型组大鼠给予LBSL(25mg/kg)治疗4天。
结果:体外结果显示LBSL(10μM)促进细胞增殖和迁移,影响细胞周期的S期。Westernblot信号显示LBSL提高了occludin的表达水平。LBSL治疗后miR-195-3p水平降低,这可以通过转染miR-195-3p模拟物来逆转,证明LBSL抑制miR-195-3p以改善细胞生长。体内结果显示,LBSL能逆转黏膜下层萎缩的绒毛和炎症细胞浸润,恢复miR-195-3p,occludin,禁食组小鼠肠道中的Ki67水平。
结论:LBSL通过降低miR-195-3p的表达来恢复受损的肠上皮。