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作 者:米凯 黄锐[2] Mi Kai;Huang Rui(416 Hospital of Nuclear Industry,the Second Affiliated Hospital of Chengdu Medical College,Chengdu,Sichuan 610051;Sichuan Provincial People′s Hospital,Sichuan Academy of Medical Sciences,Chengdu,Sichuan 610072,China)
机构地区:[1]成都医学院第二附属医院·核工业四一六医院,四川成都610051 [2]四川省医学科学院·四川省人民医院,四川成都610072
出 处:《四川医学》2020年第2期142-146,共5页Sichuan Medical Journal
摘 要:目的基于TGF-β/Smad信号通路研究芒果苷对肝纤维化大鼠的作用机制。方法健康SD大鼠40只随机分为5组,包括空白组、模型组、芒果苷低剂量组、芒果苷中剂量组及芒果苷高剂量组。除空白组外,其余组采用四氯化碳诱导肝纤维化大鼠模型,造模成功后,芒果苷低、中、高剂量组分别以15mg/kg、30mg/kg、60mg/kg芒果苷生理盐水溶液灌胃,空白组、模型组等量生理盐水灌胃,1次/d,连续6周,待最后一次给药72h后眼眶取血并处死动物,采样。HE、Masson染色观察肝组织病理学改变;ELISA检测血清TGF-β1、HA、HYP、SOD水平;免疫组化检测肝脏组织Collagen I、α-SMA、Smad2、TGF-β的表达;RT-PCR检测肝脏组织中Smad2、TGF-β、MCP-1 mRNA表达。结果HE和Masson染色结果显示芒果苷高剂量组可明显减轻肝脏组织病理损伤;与模型组相比,仅芒果苷高剂量组能明显降低TGF-β1、HA、HYP、Collagen I、α-SMA、Smad2、TGF-β、MCP-1水平,明显升高SOD水平,差异有统计学意义(P<0.05)。结论芒果苷具有抑制大鼠肝纤维化作用,其机制可能与减轻炎症反应保护肝功能,抑制TGF-β/Smad信号通路有关。Objective To study the mechanism of mangiferin on liver fibrosis in rats based on TGF-β/Smad signaling pathway.Methods Forty healthy SD rats were randomly divided into 5 groups,including the blank group,the model group,the low-dose mangiferin group,the middle-dose group,and the high-dose group.Except the blank group,the other groups used carbon tetrachloride to induce liver fibrosis in rat models.After successful modeling,the mangoside low,medium,and high dose groups were 15 mg/kg,30 mg/kg,and 60 mg/kg respectively mangiferin physiological saline solution was administered to the stomach,the blank group and the model group were administered the same amount of normal saline once per day for 6 consecutive weeks.After 72 hours of the last administration,blood was taken from the orbital and the animals were sacrificed and sampled.HE and Masson staining to observe the pathological changes of liver tissue,ELISA to detect the levels of serum TGF-β1,HA,HYP,SOD,immunohistochemical detection of liver tissue collagen I,α-SMA,Smad2,TGF-βexpression,RT-PCR to detect Smad2,TGF-β,MCP-1 mRNA expression in liver tissue.Results HE and Masson staining results show that high doses of mangiferin can significantly reduce liver pathological damage.Compared with the model group,only the high-dose mangiferin group significantly reduced the levels of TGF-β1,HA,HYP,Collagen I,α-SMA,Smad2,TGF-β,and MCP-1,and significantly increased SOD levels(P<0.05).Conclusion Mangiferin can inhibit liver fibrosis in rats,and its mechanism may be related to reducing inflammatory response and protecting liver function,and inhibiting TGF-β/Smad signaling pathway.
关 键 词:肝纤维化 芒果苷 TGF-Β/SMAD信号通路 大鼠
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