中国医药导报
中國醫藥導報
중국의약도보
CHINA MEDICAL HERALD
2014年
29期
15-18,27
,共5页
孟晓华%董科%徐湜潺%冯晓明%田晓%史国辉
孟曉華%董科%徐湜潺%馮曉明%田曉%史國輝
맹효화%동과%서식잔%풍효명%전효%사국휘
肝细胞生长因子%双环醇%肾间质纤维化%转化生长因子-β1
肝細胞生長因子%雙環醇%腎間質纖維化%轉化生長因子-β1
간세포생장인자%쌍배순%신간질섬유화%전화생장인자-β1
Hepatocyte growth factor%Bicyclol%Renal interstitial fibrosis%TGF-β1
目的:观察单侧输尿管梗阻(UUO)模型大鼠在双环醇的干预下,肝细胞生长因子(HGF)、转化生长因子-β1(TGF-β1)表达的动态变化,探讨双环醇延缓肾间质纤维化的可能机制。方法将60只雄性SD大鼠随机分为3组:假手术组、模型组、双环醇组,每组各20只,建立单侧输尿管梗阻模型。双环醇组于术前2 d给予双环醇[200 mg/(kg·d)]灌胃,假手术组、模型组给予等量自来水灌胃。每组分别在术后3、6、9、14 d时随机处死5只大鼠并取左侧肾组织,行HE染色观察肾组织病理变化,免疫组织化学染色观察HGF、TGF-β1蛋白的表达,RT-PCR法检测肾组织HGF mRNA的表达水平。结果模型组中HGF蛋白及mRNA表达均呈现早期升高后期降低的趋势,在第6天表达量最高,随后逐渐下降,表达量在术后3、9、14 d与术后6 d比较差异有高度统计学意义(P<0.01)。而TGF-β1蛋白的表达量呈现随梗阻时间延长逐渐升高趋势,术后3、6、9 d与术后14 d比较,差异有高度统计学意义(P<0.01)。在相同时间点,双环醇组与模型组相比,HGF蛋白及mRNA表达量显著升高,差异有高度统计学意义(P<0.01),而TGF-β1蛋白表达量显著降低,差异有统计学意义(P<0.01)。结论双环醇通过上调HGF及下调TGF-β1的表达而发挥缓解肾间质纤维化的作用。
目的:觀察單側輸尿管梗阻(UUO)模型大鼠在雙環醇的榦預下,肝細胞生長因子(HGF)、轉化生長因子-β1(TGF-β1)錶達的動態變化,探討雙環醇延緩腎間質纖維化的可能機製。方法將60隻雄性SD大鼠隨機分為3組:假手術組、模型組、雙環醇組,每組各20隻,建立單側輸尿管梗阻模型。雙環醇組于術前2 d給予雙環醇[200 mg/(kg·d)]灌胃,假手術組、模型組給予等量自來水灌胃。每組分彆在術後3、6、9、14 d時隨機處死5隻大鼠併取左側腎組織,行HE染色觀察腎組織病理變化,免疫組織化學染色觀察HGF、TGF-β1蛋白的錶達,RT-PCR法檢測腎組織HGF mRNA的錶達水平。結果模型組中HGF蛋白及mRNA錶達均呈現早期升高後期降低的趨勢,在第6天錶達量最高,隨後逐漸下降,錶達量在術後3、9、14 d與術後6 d比較差異有高度統計學意義(P<0.01)。而TGF-β1蛋白的錶達量呈現隨梗阻時間延長逐漸升高趨勢,術後3、6、9 d與術後14 d比較,差異有高度統計學意義(P<0.01)。在相同時間點,雙環醇組與模型組相比,HGF蛋白及mRNA錶達量顯著升高,差異有高度統計學意義(P<0.01),而TGF-β1蛋白錶達量顯著降低,差異有統計學意義(P<0.01)。結論雙環醇通過上調HGF及下調TGF-β1的錶達而髮揮緩解腎間質纖維化的作用。
목적:관찰단측수뇨관경조(UUO)모형대서재쌍배순적간예하,간세포생장인자(HGF)、전화생장인자-β1(TGF-β1)표체적동태변화,탐토쌍배순연완신간질섬유화적가능궤제。방법장60지웅성SD대서수궤분위3조:가수술조、모형조、쌍배순조,매조각20지,건립단측수뇨관경조모형。쌍배순조우술전2 d급여쌍배순[200 mg/(kg·d)]관위,가수술조、모형조급여등량자래수관위。매조분별재술후3、6、9、14 d시수궤처사5지대서병취좌측신조직,행HE염색관찰신조직병리변화,면역조직화학염색관찰HGF、TGF-β1단백적표체,RT-PCR법검측신조직HGF mRNA적표체수평。결과모형조중HGF단백급mRNA표체균정현조기승고후기강저적추세,재제6천표체량최고,수후축점하강,표체량재술후3、9、14 d여술후6 d비교차이유고도통계학의의(P<0.01)。이TGF-β1단백적표체량정현수경조시간연장축점승고추세,술후3、6、9 d여술후14 d비교,차이유고도통계학의의(P<0.01)。재상동시간점,쌍배순조여모형조상비,HGF단백급mRNA표체량현저승고,차이유고도통계학의의(P<0.01),이TGF-β1단백표체량현저강저,차이유통계학의의(P<0.01)。결론쌍배순통과상조HGF급하조TGF-β1적표체이발휘완해신간질섬유화적작용。
Objective To observe the dynamic change of hepatocyte HGF and TGF-β1 of UUO rats intervened by bicy-clol, in order to discuss the possible mechanism of renal interstitial fibrosis delayed by bicyclol. Methods 60 male SD rats were randomly divided into sham-operated group (SOR), UUO model group and bicyclol-treated group (BIC), each group had 20 rats. Through ligating the left ureter, the unilateral ureteral obstructive rat model was established. 2 days before surgery, the rats in bicyclol-treated group were administed with bicyclol [200 mg/(kg·d)]. Rats in the sham-op-erated group and the model group were administed with tap water. Rats were sacrificed after the surgery for 3, 6, 9 and 14 days. The left kidney was taken. RT-PCR was used to detect the expression of HGF mRNA in renal tissue. The ex-pression of HGF and TGF-β1 protein were measured by immunohistochemistry. HE stain was used to examine the area of pathological changes. Results In model group, the mRNA and protein expression levels of HGF increased markedly on day 3 and reached its peak value on day 6 after the surgery, then slowly fallen down, and the expression levels on day 6 were significantly different between on day 3, 9, 14 after the surgery, the differences were statistically significant (P< 0.01). However, the protein expression levels of TGF-β1 increased with extension of obstruction, and the expres-sion levels on day 14 were significantly different from on day 3, 6, 9 after the surgery, the differences were statistically significant (P< 0.01). At each research point, the mRNA and protein expression levels of HGF were significantly high-er in the bicyclol-treated group than those in the model group, the differences were statistically significant (P< 0.01). The protein expression level of TGF-β1 was significantly lower in the bicyclol-treated group than that in the model group, the difference was statistically significant (P<0.01). Conclusion Bicyclol can alleviate the degree of renal inter-stitial fibrosis through increasing the expression of HGF and decreasing the expression of TGF-β1.