首页|基于JAK/STAT信号通路探讨"敛疮生肌方"灌肠疗法对UC模型大鼠结肠黏膜屏障的作用

基于JAK/STAT信号通路探讨"敛疮生肌方"灌肠疗法对UC模型大鼠结肠黏膜屏障的作用

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目的 探讨敛疮生肌灌肠疗法调控JAK/STAT信号通路对溃疡性结肠炎(Ulcerative colitis,UC)模型大鼠结肠损伤和黏膜屏障的影响。方法 2,4,6-三硝基苯磺酸/乙醇法建立溃疡性结肠炎大鼠模型,随机分为正常对照组(不造模)、模型组、阳性药组(美沙拉嗪缓释颗粒0。42 g·kg-1)、敛疮生肌方高(灌肠10。5 g·kg-1)、中(灌肠5。25 g·kg-1)、低剂量组(灌肠2。62g·kg-1)。比较各组大鼠粪便隐血、结肠黏膜损伤程度、病理变化情况,Western blot法检测UC模型大鼠结肠组织JAK2、p-JAK2、STAT3、p-STAT3蛋白表达量,TUNEL观察结肠组织凋亡情况。结果 实验结果表明,美沙拉嗪组、敛疮生肌方中、高剂量组可缓解大鼠体质量下降,降低粪便隐血评分,改善结肠受损程度,减轻结肠溃疡区黏膜层、黏膜下层炎性细胞浸润和黏膜层坏死程度;美沙拉嗪组、敛疮生肌低、中、高剂量组可不同程度下调p-JAK2、p-STAT3蛋白表达量(与模型组比较,P<0。05),其中以高剂量组最为显著(P<0。01);结肠组织凋亡率明显降低(P<0。05)。结论 敛疮生肌灌肠疗法能够明显改善溃疡性结肠炎大鼠的便血、结肠病理损伤程度,其机制可能与抑制JAK2、STAT3磷酸化蛋白表达,进一步抑制JAK/STAT信号通路有关。
Exploring the Effect of Enema Therapy for Constraining Sores and Promoting Tissue Regeneration on the Colonic Mucosal Barrier in Rats with Ulcerative Colitis Based on the JAK/STAT Signaling Pathway
Objective To explore the effects of the regulation of JAK/STAT signaling pathway by the therapy of astringent ulcer and muscle inducing enema on colon injury and mucosal barrier in ulcerative colitis(UC)model rats.Methods A rat model of ulcerative colitis was established using 2,4,6-trinitrobenzenesulfonic acid/ethanol method.The model was randomly divided into a normal control group(without modeling),a model group,a positive drug group(mesalazine sustained-release granules 0.42 g·kg-1),a high dose of Lianchuang Shengji Formula(enema 10.5 g·kg-1),a medium dose(enema 5.25 g·kg-1),and a low dose group(enema 2.62 g·kg-1).Compare the fecal occult blood,degree of colonic mucosal damage,and pathological changes of rats in each group,and detect the expression of JAK2,STAT3 proteins,and their phosphorylated proteins in colon tissue using Western blot method.Results The results showed that the mesalazine group,the medium and high-dose groups of Lianchuang Shengji Formula could increase the body mass of rats,reduce fecal occult blood score,improve colon damage,and achieve pathological results;The mesalazine group and the low,medium,and high dose groups of Lianchuang Shengji can downregulate the expression of p-JAK2 and p-STAT3 proteins(compared with the model group,P<0.05),with the high-dose group being the most significant(P<0.01).The apoptosis rate of colon tissue significantly decreased(P<0.05).Conclusion The enema therapy of astringent ulcer and promoting muscle growth can significantly improve the pathological scores of bloody stools and colon injury in rats with ulcerative colitis.The mechanism may be related to the inhibition of JAK2 and STAT3 phosphorylation protein expression,and further inhibition of the JAK/STAT signaling pathway.

Conquering sore and promoting muscle enemaUlcerative colitisMucosal barrierJAK2/STAT3 signaling pathway

刘竺华、张彩峰、皇菊莲、薛雯娣

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山西中医药大学附属医院 太原 030024

山西省药品审评中心·山西省医药与生命科学研究院 太原 030006

敛疮生肌灌肠 溃疡性结肠炎 黏膜屏障 JAK2/STAT3信号通路

2024

世界科学技术-中医药现代化
中科院科技政策与管理科学研究所,中国高技术产业发展促进会

世界科学技术-中医药现代化

CSTPCD北大核心
影响因子:1.175
ISSN:1674-3849
年,卷(期):2024.26(11)