国际中医中药杂志
國際中醫中藥雜誌
국제중의중약잡지
INTERNATIONAL JOURNAL OF TRIDITIONAL CHINESE MEDICINE
2013年
10期
893-895
,共3页
补脾益肾法%阿霉素诱导慢性肾损害%细胞周期蛋白激酶抑制剂p21%转化生长因子β1
補脾益腎法%阿黴素誘導慢性腎損害%細胞週期蛋白激酶抑製劑p21%轉化生長因子β1
보비익신법%아매소유도만성신손해%세포주기단백격매억제제p21%전화생장인자β1
Reinforcing spleen and kidney%Adriamycin-induced CKD%Cyclin-dependent kinase inhibitor p21cip1%Transforming growth factor-β1
目的 研究补脾益肾中药对阿霉素诱导大鼠慢性肾损害肾脏病变的影响,探讨其对肾间质纤维化和肾小球硬化的延缓作用.方法 健康雄性SD大鼠36只,随机分为模型组和空白对照组；模型建立后,模型组大鼠又随机分为模型对照组、苯那普利组和中药低、中、高剂量组;观察造模后第14天、第28天、第42天各组大鼠的一般情况、生化指标,第42天实验结束时处死大鼠取肾,用免疫组织化学染色方法测定各组大鼠肾组织中p21、TGF-β1表达的变化.结果 阿霉素诱导大鼠慢性肾损害的大鼠7天后出现蛋白尿,14d尿蛋白排泄达到高峰；中药治疗组、苯那普利组均明显降低阿霉素肾病大鼠的24 h尿蛋白量(P＜0.05),其中中药高剂量组疗效更显著；肾组织病理切片示模型组大鼠肾组织中p21 (518886.35±6810.89)和TGF-β1 (222012.95±50484.73)表达明显增加(P＜0.05);中药高剂量治疗组p21 (288627.66±97021.65)和TGF-β1(98405.14±19216.89)表达明显低于模型对照组(P＜0.05).结论 补脾益肾法中药复方制剂可能通过调节肾组织中p21和TGF-β1的表达以减少蛋白尿从而保护肾脏,延缓肾脏病的进展.
目的 研究補脾益腎中藥對阿黴素誘導大鼠慢性腎損害腎髒病變的影響,探討其對腎間質纖維化和腎小毬硬化的延緩作用.方法 健康雄性SD大鼠36隻,隨機分為模型組和空白對照組；模型建立後,模型組大鼠又隨機分為模型對照組、苯那普利組和中藥低、中、高劑量組;觀察造模後第14天、第28天、第42天各組大鼠的一般情況、生化指標,第42天實驗結束時處死大鼠取腎,用免疫組織化學染色方法測定各組大鼠腎組織中p21、TGF-β1錶達的變化.結果 阿黴素誘導大鼠慢性腎損害的大鼠7天後齣現蛋白尿,14d尿蛋白排洩達到高峰；中藥治療組、苯那普利組均明顯降低阿黴素腎病大鼠的24 h尿蛋白量(P＜0.05),其中中藥高劑量組療效更顯著；腎組織病理切片示模型組大鼠腎組織中p21 (518886.35±6810.89)和TGF-β1 (222012.95±50484.73)錶達明顯增加(P＜0.05);中藥高劑量治療組p21 (288627.66±97021.65)和TGF-β1(98405.14±19216.89)錶達明顯低于模型對照組(P＜0.05).結論 補脾益腎法中藥複方製劑可能通過調節腎組織中p21和TGF-β1的錶達以減少蛋白尿從而保護腎髒,延緩腎髒病的進展.
목적 연구보비익신중약대아매소유도대서만성신손해신장병변적영향,탐토기대신간질섬유화화신소구경화적연완작용.방법 건강웅성SD대서36지,수궤분위모형조화공백대조조；모형건립후,모형조대서우수궤분위모형대조조、분나보리조화중약저、중、고제량조;관찰조모후제14천、제28천、제42천각조대서적일반정황、생화지표,제42천실험결속시처사대서취신,용면역조직화학염색방법측정각조대서신조직중p21、TGF-β1표체적변화.결과 아매소유도대서만성신손해적대서7천후출현단백뇨,14d뇨단백배설체도고봉；중약치료조、분나보리조균명현강저아매소신병대서적24 h뇨단백량(P＜0.05),기중중약고제량조료효경현저；신조직병리절편시모형조대서신조직중p21 (518886.35±6810.89)화TGF-β1 (222012.95±50484.73)표체명현증가(P＜0.05);중약고제량치료조p21 (288627.66±97021.65)화TGF-β1(98405.14±19216.89)표체명현저우모형대조조(P＜0.05).결론 보비익신법중약복방제제가능통과조절신조직중p21화TGF-β1적표체이감소단백뇨종이보호신장,연완신장병적진전.
Objective To investigate the effect of reinforcing spleen and kidney method on adriamycin-induced CKD in rats and to explore its possible mechanism.Methods Totally 36 Sprague-Dawley rats were randomly divided into a Adriamycin-induced model group and a control group.The model group was further divided into five groups:the Adriamycin-induced model control group,bennazepril-treated group,and TCM treated low,moderate,and high dose groups.The level of serum creatinine,urea nitrogen,24hours urine protein and urine creatinine were measured at 14,28,42 days after establishing the model rats.And the protein expression of transforming growth factor-β1 (TGF-β1) and cyclin-dependent kinase inhibitor p21cip1 (p21)were detected by immunohistochemistry.Results The proteinuria was observed on the seventh day after injection of adriamycin in adriamycin nephropathy model group,and reached summit on the fourteenth day.Both TCM treated groups and benazepril group reduced the level of urine protein within 24 hours (P＜0.05),the reduction was most remarkable in the TCM high dose group.The expression of p21 and TGF-β1 (p21 288627.66±97021.65,TGF-β1 98405.14± 19216.89) in kidney increased in the model groups,while the TCM treated high dose group (p21 518886.35±6810.89,TGF-β1 222012.95± 50484.73) was significantly lower than the model control group (P＜ 0.05).Conclusion Reinforcing spleen and kidney method could decrease the level of urine protein within 24 hours by regulating the expression of p21 and TGF-β1,so thus to protect renal function and delay progress of kidney disease.
