Abstract：
BACKGROUND: The fruit of Lycium barbarum L. is widely employed with the traditional effect of tonic properties. According to the theory of traditional Chinese medicine, Gou Qi can be distributed in the meridian of stomach, as well as the liver and kidney, indicating its effect on the digestive system. Clinical studies found that Gou Qi enhanced gastrointestinal functions. Pharmacological research showed the extract of Lycium barbarum exhibiting a repaired effect on the intestine barrier. Lycibarbarspermidine L (LBS L), which belongs to polyamines, is separated from the fruit of Lycium barbarum. However, it is unknown whether LBS L can restore damaged intestinal barrier like other polyamines such as spermidine.
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.
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.
摘要：
背景：枸杞果实被广泛使用，具有传统的滋补特性。根据中医理论,勾气可以分布在胃的经络，以及肝脏和肾脏，表明其对消化系统的影响。临床研究发现，勾气增强胃肠功能。药理研究表明，枸杞提取物对肠屏障具有修复作用。利西巴亚精胺L（LBSL），属于多胺，是从枸杞果实中分离出来的。然而,目前尚不清楚LBSL能否像亚精胺等其他多胺一样恢复受损的肠屏障。
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。
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。
