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作 者:王东[1] 张长明[2] 王云满[3] 何立群[1,4]
机构地区:[1]上海中医药大学附属曙光医院,上海市普安路185号200021 [2]上海中医药大学附属市中医院 [3]上海中医药大学附属普陀医院 [4]上海市中医临床重点实验室
出 处:《中医杂志》2013年第5期420-423,共4页Journal of Traditional Chinese Medicine
基 金:"十一五"国家科技重大专项资助项目(2009ZX09311-003);国家自然科学基金资助项目(81173219);科技部中医药行业科研专项资助项目(201007005);高等学校博士学科点专项科研基金资助项目(20093107110006);上海市科委创新行动计划项目(11DZ1973100);上海高校创新团队建设项目(第二期)
摘 要:目的探讨抗纤灵方对肾间质纤维化(RIF)的作用机制。方法将抗纤灵方煎至含生药3.2g/ml、福辛普利0.33mg/ml给大鼠灌胃,正常组给予等量蒸馏水灌胃,分别制备抗纤灵方血清、福辛普利血清和正常血清。用DMEM培养基稀释血清,分为正常血清组、福辛普利组、抗纤灵组、转化生长因子-β1(TGF-β1)组、TGF-β1+福辛普利组和TGF-β1+抗纤灵组。体外培养大鼠肾组织骨髓来源的成纤维细胞(FBS),采用酶联免疫吸附法和双重荧光定量法检测骨髓来源的FBS表型转化标记物α-平滑肌肌动蛋白(α-SMA)及Ⅰ型胶原(CollagenⅠ)及其mRNA表达。结果 TGF-β1组α-SMA、CollagenⅠ及α-SMAmRNA、CollagenⅠmRNA表达水平较正常血清组明显增强(P<0.05或P<0.01),TGF-β1+福辛普利组和TGF-β1+抗纤灵组α-SMA、CollagenⅠ及α-SMAmRNA、CollagenⅠmRNA表达水平均低于TGF-β1组(P<0.05或P<0.01)。结论抗纤灵方药物血清可以通过抑制骨髓来源的FBS的表型转化拮抗RIF。Objective To study the effect and mechanism of Kangxianling on renal interstitial fibrosis (RIF). Methods Kangxianling serum, fosinopril serum and normal serum was prepared respectively with intragastric administration of 3.2 g/ml Kangxianling, 3.3 mg/mI fosinopril and distilled water to rats. The serum was diluted with a DMEM medium and divided into the normal group, fosinopril group, Kangxianling group, transforming growth factor-β1 (TGF-β1) group, TGF-β1 + fosinopril group and TGF-β1 +Kangxianling group. The bone marrow-derived fetal bovine serum (FBS) was studied. The expressions of a-smooth muscle actin (a-SMA) and Collagen I were examined by enzyme-linked immunosorbent assay (ELISA) and real time polymerase chain reaction (RT-PCR). Results Comparing with the normal group, the expressions of a-SMA, Collagen I, a- SMA mRNA and Collagen I mRNA were significantly improved in the TGF-β1 group (P〉0.05 or P〈0.01). Comparing with the TGF-β1 group, the expressions of a-SMA, Collagen I, a-SMA mRNA and Collagen I mRNA were significantly decreased in the TGF-β1t+fosinopril group and TGF-β1+Kangxianling group (P〈0.05 or P〈0. 01). Conclusion fKangxianling can antagonize RIF by inhibiting phenotypic transformation of bone marrow-derived FBS.
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