| 李玉龙,闫春英,吕颐菲,张玲瑞,宗 伟.芍药苷对溃疡性结肠炎大鼠肠道屏障功能和ERK信号通路的影响[J].,2022,(15):2829-2835 |
| 芍药苷对溃疡性结肠炎大鼠肠道屏障功能和ERK信号通路的影响 |
| Effect of Paeoniflorin on the Intestinal Barrier Function and ERK Signal Pathway in Rats with Ulcerative Colitis |
| 投稿时间：2021-10-23 修订日期：2021-11-18 |
| DOI：10.13241/j.cnki.pmb.2022.15.006 |
| 中文关键词: 溃疡性结肠炎 芍药苷 结肠粘液 肠道屏障功能 ERK信号通路 |
| 英文关键词: Ulcerative colitis Paeoniflorin Colonic mucus Intestinal barrier function ERK signaling pathway |
| 基金项目:陕西省自然科学基础研究计划项目（2020JM-654） |
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| 中文摘要: |
| 摘要 目的：探究芍药苷对溃疡性结肠炎（UC）发生过程中肠道屏障功能和ERK信号通路的影响。方法：将24只7-8周龄SPF级雄性SD大鼠随机分为4组：正常组（Normal组，未造模及给药的大鼠）、模型组（Model组，100 mg/kg TNBS给药造模）、低剂量芍药苷组（LPF组，100 mg/kg TNBS +10 mg/kg芍药苷给药处理）和高剂量芍药苷组（HPF组，100 mg/kg TNBS +100 mg/kg芍药苷给药处理），每组6只大鼠。对大鼠推注5%三硝基苯磺酸（TNBS）进行UC大鼠造模，然后灌胃指定浓度的芍药苷，连续处理14 d。通过苏木精伊红（HE）染色进行组织病理学观察，通过阿尔辛蓝（AB）染色计算结肠粘液层厚度。通过ELISA法检测结肠组织中细胞因子（IL-6、IL-1β、TNF-α和IL-10）、髓过氧化物酶（MPO）和粘蛋白（MUC2和MUC5AC）的水平。通过免疫组化检测各组大鼠结肠组织中IL-6和IL-10的蛋白表达。通过Western blotting分析蛋白激酶Cα（PKCα）、p-PKCα、ERK1/2和p-ERK1/2的蛋白表达。结果：与Model组（8.38±0.42 cm）相比，LPF组（9.88±0.49 cm）和HPF组（10.92±0.55 cm）UC大鼠的结肠长度显著增加（P<0.05）。与Model组（22.54±1.13 μm）相比，LPF组（41.07±2.05 μm）和HPF组（50.33±2.52 μm）UC大鼠结肠粘液层厚度显著增加（P<0.05）。与Model组相比，LPF组和HPF组UC大鼠的结肠形态明显改善，结肠组织中IL-6、IL-1β、TNF-α和MPO的水平显著降低，而IL-10显著升高（P<0.05）。与Model组相比，LPF组和HPF组UC大鼠结肠组织中MUC2和MUC5AC水平均显著升高，p-PKCα和p-ERK1/2的磷酸化水平也显著升高（P<0.05）。结论：芍药苷抑制了TNBS诱导的UC大鼠结肠炎症并增加了结肠粘液层厚度，从而保护了肠道屏障功能，其机制可能与ERK信号通路的激活有关。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect of paeoniflorin on the intestinal barrier function and ERK signaling pathway during the occurrence of ulcerative colitis (UC). Methods: Twenty-four SPF male Sprague-Dawley (SD) rats aged 7-8 weeks were randomly divided into 4 groups: normal group (Normal group, rats without modeling and administration), TNBS model group (Model group, 100 mg/kg TNBS administration model), low-dose paeoniflorin group (LPF group, 100 mg/kg TNBS + 10 mg/kg paeoniflorin administration treatment), high-dose paeoniflorin group (HPF group, 100 mg/kg TNBS + 100 mg/kg paeoniflorin administration treatment), Each group had 6 rats. Rats were given a bolus injection of 5% trinitrobenzene sulfonic acid (TNBS) for UC modeling, and then the designated concentration of paeoniflorin was intragastrically administered. Continuous treatment for 14 d. Histopathological observation was performed by hematoxylin and eosin (HE) staining, and the thickness of colon mucus layer was calculated by alcian blue (AB) staining. The levels of cytokines (IL-6, IL-1β, TNF-α and IL-10), myeloperoxidase (MPO) and mucin (MUC2 and MUC5AC) in colon tissue was analyzed by ELISA. The protein expression of IL-6 and IL-10 in the colon tissue of rats in each group was detected by immunohistochemistry. The protein expression of protein kinase Cα (PKCα), p-PKCα, ERK1/2 and p-ERK1/2 was analyzed by Western blotting. Results: Compared with Model group(8.38±0.42 cm), the colon length of UC rats in LPF group(9.88±0.49 cm) and HPF group (10.92±0.55 cm) increased significantly(P<0.05). Compared with Model group(22.54±1.13 μm), the thickness of the colonic mucus layer of UC rats in LPF group (41.07±2.05 μm) and HPF group (50.33±2.52 μm) increased significantly(P<0.05). Compared with Model group, the colon morphology of the UC rats in LPF group and HPF group was significantly improved, the levels of IL-6, IL-1β, TNF-α and MPO in the colon tissue were significantly reduced, while IL-10 was significantly increased(P<0.05). Compared with Model group, the levels of MUC2 and MUC5AC in the colon tissue of UC rats in the LPF group and the HPF group were significantly increased, and the phosphorylation levels of p-PKCα and p-ERK1/2 were also significantly increased(P<0.05). Conclusion: Paeoniflorin inhibits TNBS-induced colonic inflammation in UC rats and increases the thickness of the colonic mucus layer, thereby protecting the intestinal barrier function, the mechanism may be related to the activation of the ERK signaling pathway. |
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