中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2012年
4期
326-329
,共4页
钟海平%刘苏娅%李国法%吕惠卿%郑红斌
鐘海平%劉囌婭%李國法%呂惠卿%鄭紅斌
종해평%류소아%리국법%려혜경%정홍빈
膳食纤维%直肠结肠炎%结直肠肿瘤%细胞凋亡%胰岛素样生长因子结合蛋白类
膳食纖維%直腸結腸炎%結直腸腫瘤%細胞凋亡%胰島素樣生長因子結閤蛋白類
선식섬유%직장결장염%결직장종류%세포조망%이도소양생장인자결합단백류
Maixiansan%Proctocolitis%Colorectal neoplasms%Apoptosis%Insulin-like growth factor binding proteins
目的 探讨麦纤散对溃疡性结肠炎相关性结直肠癌实验大鼠结肠组织胰岛素样生长因子结合蛋白7(insulin-like growth factor binding protein 7,IGFBP7)基因表达及结肠肿瘤细胞凋亡的影响. 方法 将40只SD大鼠随机分为4组:空白组、模型组、麦纤散组与美莎拉嗪组；除空白组外,其余3组使用葡聚糖硫酸钠联合氧化偶氮甲烷的化学方法建立溃疡性结肠炎相关性结直肠癌大鼠模型,并分别应用药物干预,于16周后处死取结直肠,采用原位末端标记法(TUNED和实时荧光定量PCR技术分别检测大鼠结直肠肿瘤细胞凋亡率及结肠组织IGFBP7基因表达. 结果 结肠肿瘤细胞凋亡指数麦纤散组(8.70±3.47)和美莎拉嗪组(1.20±0.26)与模型组(0.38±0.11)比较均提高,麦纤散组与模型组比较,差异有统计学意义(P＜0.05)；麦纤散组结肠组织IGFBP7基因表达为50.5±14.0,与模型组18.0±3.9比较明显增加,差异有统计学意义(P＜0.05). 结论 麦纤散能对抗溃疡性结肠炎相关性结肠癌的发生与发展,其机制与促进肿瘤细胞凋亡、增加结肠组织IGFBP7表达有关.
目的 探討麥纖散對潰瘍性結腸炎相關性結直腸癌實驗大鼠結腸組織胰島素樣生長因子結閤蛋白7(insulin-like growth factor binding protein 7,IGFBP7)基因錶達及結腸腫瘤細胞凋亡的影響. 方法 將40隻SD大鼠隨機分為4組:空白組、模型組、麥纖散組與美莎拉嗪組；除空白組外,其餘3組使用葡聚糖硫痠鈉聯閤氧化偶氮甲烷的化學方法建立潰瘍性結腸炎相關性結直腸癌大鼠模型,併分彆應用藥物榦預,于16週後處死取結直腸,採用原位末耑標記法(TUNED和實時熒光定量PCR技術分彆檢測大鼠結直腸腫瘤細胞凋亡率及結腸組織IGFBP7基因錶達. 結果 結腸腫瘤細胞凋亡指數麥纖散組(8.70±3.47)和美莎拉嗪組(1.20±0.26)與模型組(0.38±0.11)比較均提高,麥纖散組與模型組比較,差異有統計學意義(P＜0.05)；麥纖散組結腸組織IGFBP7基因錶達為50.5±14.0,與模型組18.0±3.9比較明顯增加,差異有統計學意義(P＜0.05). 結論 麥纖散能對抗潰瘍性結腸炎相關性結腸癌的髮生與髮展,其機製與促進腫瘤細胞凋亡、增加結腸組織IGFBP7錶達有關.
목적 탐토맥섬산대궤양성결장염상관성결직장암실험대서결장조직이도소양생장인자결합단백7(insulin-like growth factor binding protein 7,IGFBP7)기인표체급결장종류세포조망적영향. 방법 장40지SD대서수궤분위4조:공백조、모형조、맥섬산조여미사랍진조；제공백조외,기여3조사용포취당류산납연합양화우담갑완적화학방법건립궤양성결장염상관성결직장암대서모형,병분별응용약물간예,우16주후처사취결직장,채용원위말단표기법(TUNED화실시형광정량PCR기술분별검측대서결직장종류세포조망솔급결장조직IGFBP7기인표체. 결과 결장종류세포조망지수맥섬산조(8.70±3.47)화미사랍진조(1.20±0.26)여모형조(0.38±0.11)비교균제고,맥섬산조여모형조비교,차이유통계학의의(P＜0.05)；맥섬산조결장조직IGFBP7기인표체위50.5±14.0,여모형조18.0±3.9비교명현증가,차이유통계학의의(P＜0.05). 결론 맥섬산능대항궤양성결장염상관성결장암적발생여발전,기궤제여촉진종류세포조망、증가결장조직IGFBP7표체유관.
Objective To invcstigate the effects of Maixiansan on insulin-like growth factor binding protein 7 (IGFBP7) and apoptosis in rats with ulcerative colitis related colorectal cancer.Methods The rat model of ulcerative colitis-related coloreetal cancer was induced by dextran sulfate sodium (DSS) and azoxymethane(AOM). 40 male SD rats [weight (160 ± 10) g] were randomly divided into 4 groups: model, Maixiansan and Meisalazine treatment as well as normal group peritoneally irjected with saline.The expression of IGFBP7 and apoptosis in coloreetal tissue were detected by real-time PCR and TUNEL after 16 weeks. Results The numbers of colorectal cancer in model group( 1.2 ± 0.4 ),in Maixiansan group ( 0.70 ± 0.15 ),in Meisalazine group ( 0.60 ± 0.16 )were higher than in normal control (P ＜ 0.05), but no differences were found among model,Maixiansan and Meisalazine groups(P＞0.05).The apoptosis in colonic mucosa for Meixiansan(8.70±3.47) group and Mesalazine group were enhanced as compared with that in model group( 1.20 ±0.26 vs.0.38±0.11,P＜0.05).The mRNA expression of IGFBP7 in colon for Meixiansan group were higher than those in model group,Meisalazine group,and normal control(50.5 ± 14.0 vs.18.0 ±3.9 and 39.3±11.4,46.4±6.0,P＜0.05). Conclusions Maixiansan may resist the occurrence and development of ulcerative colitis-related colorectal cancer through upregulating IGFBP7 expression of colorectal tissue and promoting apoptosis of tumor cell.
