医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2015年
5期
565-569
,共5页
望运玲%岳源%武双婵%丁虹
望運玲%嶽源%武雙嬋%丁虹
망운령%악원%무쌍선%정홍
法舒地尔%肠病,炎症性%大鼠
法舒地爾%腸病,炎癥性%大鼠
법서지이%장병,염증성%대서
Fasudil%Bowel disease,inflammatory%Rat
目的：探讨法舒地尔对三硝基苯磺酸( TNBS)诱导的结肠炎模型大鼠的治疗作用。方法斯泼累格·多雷(SD)雌性大鼠30只,随机分为正常对照组(0.9%氯化钠溶液造模+腹腔注射0.9%氯化钠溶液)、模型对照组(TNBS造模+腹腔注射0.9%氯化钠溶液)和法舒地尔组(TNBS造模+腹腔注射法舒地尔4.5 mg·kg-1),每组10只,连续给药14 d。观察法舒地尔对大鼠疾病活动指数( DAI)、结肠髓过氧化物酶( MPO)、肿瘤坏死因子-α( TNF-α)及白细胞介素1β( IL-1β)含量的影响；苏木精-伊红( HE)染色观察组织病理学变化；蛋白免疫印迹法观察结肠组织Rho激酶含量变化。结果正常对照组、模型对照组、法舒地尔组DAI评分分别为(0.00±0.00),(7.76±1.32),(3.20±0.98)分； MPO含量分别为(59.32±9.08),(96.65±16.57),(69.58±11.40) U·g-1；TNF-α含量分别为(0.15±0.11),(0.28±0.22),(0.20±0.62) ng·mL-1；IL-1β含量分别为(0.04±0.01),(0.08±0.02),(0.06±0.02) ng·mL-1；Rho激酶相对表达量分别为0.713±0.170,1.083±0.210,0.907±0.260。结论法舒地尔可能通过降低Rho激酶的表达及减少炎症因子的释放来保护结肠炎模型大鼠。 Rho激酶可能是治疗炎症性肠病的新靶标。
目的：探討法舒地爾對三硝基苯磺痠( TNBS)誘導的結腸炎模型大鼠的治療作用。方法斯潑纍格·多雷(SD)雌性大鼠30隻,隨機分為正常對照組(0.9%氯化鈉溶液造模+腹腔註射0.9%氯化鈉溶液)、模型對照組(TNBS造模+腹腔註射0.9%氯化鈉溶液)和法舒地爾組(TNBS造模+腹腔註射法舒地爾4.5 mg·kg-1),每組10隻,連續給藥14 d。觀察法舒地爾對大鼠疾病活動指數( DAI)、結腸髓過氧化物酶( MPO)、腫瘤壞死因子-α( TNF-α)及白細胞介素1β( IL-1β)含量的影響；囌木精-伊紅( HE)染色觀察組織病理學變化；蛋白免疫印跡法觀察結腸組織Rho激酶含量變化。結果正常對照組、模型對照組、法舒地爾組DAI評分分彆為(0.00±0.00),(7.76±1.32),(3.20±0.98)分； MPO含量分彆為(59.32±9.08),(96.65±16.57),(69.58±11.40) U·g-1；TNF-α含量分彆為(0.15±0.11),(0.28±0.22),(0.20±0.62) ng·mL-1；IL-1β含量分彆為(0.04±0.01),(0.08±0.02),(0.06±0.02) ng·mL-1；Rho激酶相對錶達量分彆為0.713±0.170,1.083±0.210,0.907±0.260。結論法舒地爾可能通過降低Rho激酶的錶達及減少炎癥因子的釋放來保護結腸炎模型大鼠。 Rho激酶可能是治療炎癥性腸病的新靶標。
목적：탐토법서지이대삼초기분광산( TNBS)유도적결장염모형대서적치료작용。방법사발루격·다뢰(SD)자성대서30지,수궤분위정상대조조(0.9%록화납용액조모+복강주사0.9%록화납용액)、모형대조조(TNBS조모+복강주사0.9%록화납용액)화법서지이조(TNBS조모+복강주사법서지이4.5 mg·kg-1),매조10지,련속급약14 d。관찰법서지이대대서질병활동지수( DAI)、결장수과양화물매( MPO)、종류배사인자-α( TNF-α)급백세포개소1β( IL-1β)함량적영향；소목정-이홍( HE)염색관찰조직병이학변화；단백면역인적법관찰결장조직Rho격매함량변화。결과정상대조조、모형대조조、법서지이조DAI평분분별위(0.00±0.00),(7.76±1.32),(3.20±0.98)분； MPO함량분별위(59.32±9.08),(96.65±16.57),(69.58±11.40) U·g-1；TNF-α함량분별위(0.15±0.11),(0.28±0.22),(0.20±0.62) ng·mL-1；IL-1β함량분별위(0.04±0.01),(0.08±0.02),(0.06±0.02) ng·mL-1；Rho격매상대표체량분별위0.713±0.170,1.083±0.210,0.907±0.260。결론법서지이가능통과강저Rho격매적표체급감소염증인자적석방래보호결장염모형대서。 Rho격매가능시치료염증성장병적신파표。
Objective To investigate the treatment effect of fasudilon inflammatory bowel disease ( IBD) in rats. IBD was induced by using an enema of trinitro-benzene-sulfonic acid ( TNBS ) . Methods A total of 30 female SD rats were randomly divided into normal control group (0. 9% sodium chloride for induction and 0. 9% sodium chloride for treatment), model control group (TNBS for induction and 0. 9% sodium chloride for treatment), and fasudil group (TNBS for induction and fasudil 4. 5 mg·kg-1 for treatment). The disease activity index(DAI) was estimated 14 days later. The MPO activity, TNF-αcontent and IL-1β level in the colon were investigated, while Rho kinase expression was detected by Western blot. The pathological changes were detected by HE staining. Results The DAI of the normal control, model control, and fasudil groups were:(0. 00±0. 00),(7. 76±1. 32),and (3. 20±0. 98), respectively. MPO activity was (59. 32±9. 08),(96. 65±16. 57),and (69. 58±11. 40) U·g-1, respectively. TNF-α was (0. 15±0. 11),(0. 28±0. 22),and (0. 20±0. 62) ng·mL-1, respectively. IL-1β content was (0. 04±0. 01),(0. 08±0. 02),and (0. 06±0. 02) ng·mL-1, respectively. Rho kinase expression was 0. 713± 0. 170,1. 083±0. 210,and 0. 907±0. 260, respectively. Conclusion Fasudil excerts protective effects against IBD in rats by lowering the expression of Rho kinase and attenuating the release of inflammatory mediators, suggesting that Rho kinase could be a new therapeutic target for IBD.
