黄芪多糖对炎症性肠病模型大鼠NFATC4表达的影响

目的 观察黄芪多糖（APS）对炎症性肠病（IBD）模型大鼠结肠黏膜NFATC4表达及受损结肠黏膜的修复作用.方法 采用三硝基苯磺酸诱导IBD大鼠模型.45只大鼠随机分为假手术组、IBD模型组、APS低剂量组（100 mg·kg-1）、APS高剂量组（200 mg·kg-1）和地塞米松对照组（地塞米松0.3 mg·kg-1）.分别给予相应药物腹腔注射,每日1次.给药7 d后,乙醚麻醉下处死大鼠,取结肠组织进行形态学及病理组织学评分,实时PCR和ELISA法检测结肠组织NFATC4 mRNA和蛋白表达.结果 各组大鼠结肠组织形态学肉眼评分为：假手术组0分、IBD模型组（5.67 ± 0.87）分、APS低剂量组（3.56 ± 0.89）分、APS高剂量组（1.56 ± 0.53）分、地塞米松对照组（0.89 ± 0.78）分,组间差异总体上有统计学意义（F=69.195,P〈0.001）.病理学评分为：假手术组（0.11± 0.08）分,IBD模型组（5.67 ± 1.15）分、APS低剂量组（3.33 ± 0.58）分、APS高剂量组（1.33 ± 1.15）分、地塞米松对照组（1.67 ± 1.52）分,组间差异总体上有统计学意义（F=13.34,P〈0.01）.组织病理学检查显示APS可修复IBD模型大鼠受损结肠黏膜.NFATC4 mRNA表达APS高剂量组、APS低剂量组与地塞米松对照组均显著高于IBD模型组（P〈0.01）;仅APS高剂量组与地塞米松对照组NFATC4蛋白表达较IBD模型组显著增加（P〈0.001）.结论 APS可增加IBD模型大鼠NFATC4表达,对损伤结肠黏膜有修复作用,APS对NFATC4调控机制尚有待进一步研究.

The effect of Astragalus polysaccharides on NFATC4 expression in a rat model of inflammatory bowel disease

Objective To investigate the effect of Astragalus polysaccharide （APS） on the expression of NFATC4 and the regulation of intestinal mucosal immune system in a rat model of inflammatory bowel disease （IBD）. Methods The IBD rat model was induced by trinitrobenzene sulfonic acid. Forty five rats were randomly divided into 5 groups： sharm group, IBD group, low-dose APS group （100 mg · kg^-1）, high-dose APS group （200 mg · kg^-1） and dexamethasone control group （dexamethasone 0. 3 mg· kg^-1 ）. The medications were administrated by intraperitoneal injection once a day for 7 days. Under anesthesia by ether, all animals were sacrificed. The colonic tissue morphological and histopathological changes were estimated by a numerical injury score system, the expression of NFATC4 mRNA was assessed by real time PCR, and the protein expression of NFATC4 was measured by an enzyme linked immunosorbent assay. Results The scores of colonic tissue morphology were： sharm group （0）, IBD group （5.67 ± 0. 87 ）, low-dose APS group （ 3.56 ± 0. 89 ）, high-dose APS group （ 1.56± 0. 53 ）, dexamethasone control group （0. 89±0. 78）. The scores of colonic tissue histopathology were： sharm group （0.11±0.08）, IBD group （5.67 ± 1.15）, low-dose APS group （3.33± 0. 58）, high-dose APS group （ 1.33 ± 1.15 ） , dexamethasone control group （ 1.67±1.52）. Both the morphological and histological scores among groups were significantly different （morphology： F = 69. 195, P 〈 0. 001; histology： F = 13.34, P 〈 0. 01 ）. Histopathological exam confirmed that APS at low and high doses significantly improved mucosal injuries of colon. Compared with IBD group, the expressions of NFATC4 mRNA were increased significantly in high-dose APS group, low-dose APS group and dexmnethasone control group （ P 〈 0.01 ） , but the protein expressions of＇ NFATC4 were significant increased only in high-dose APS group and dexamethasone contrail group （ P 〈 0. 001 ）. Conclusions APS improved colonic mtwosal injuries by increasing the expression of NFATC4 in a rat model of IBD. Further studies would be needed to investigate the underlying regulator） mechanism of APS-induced NFATC4 change.