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作 者:马广礼[1] 夏晓培 MA Guang-li;XIA Xiao-pei(College of Medical and Health,Xuchang Vocational Technical College,Xuchang 461000,China)
机构地区:[1]许昌职业技术学院医疗卫生学院,许昌461000
出 处:《天然产物研究与开发》2024年第6期938-945,共8页Natural Product Research and Development
基 金:河南省高等教育教学改革研究与实践项目(2019SJG LX716)。
摘 要:研究了灵芝多糖(Ganoderma lucidum polysaccharide,GLP)对糖尿病肾病(diabetic nephropathy,DN)小鼠的作用。成功构建DN小鼠模型后GLP干预。检测小鼠空腹血糖和24 h尿蛋白含量,测定尿素氮(blood urea nitrogen,BUN)和肌酐(serum creatinine,Scr)水平,结合伊红和马松染色观察肾脏病理形态,采用酶联免疫吸附试验测定肿瘤坏死因子α(tumor necrosis factor-alpha,TNF-α)、白细胞介素6(interleukin-6,IL-6)和白细胞介素10(interleukin-10,IL-10)的水平,使用蛋白免疫印迹法检测晚期糖基化终产品受体(receptor for advanced glycation end-products,RAGE)、Ⅳ型胶原蛋白(collagen type IV,COL-Ⅳ)和诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)蛋白的表达含量。DN组小鼠空腹血糖、24 h尿蛋白、BUN和Scr及其肾组织中TNF-α和IL-6水平均升高(P<0.05),血清中IL-10水平降低(P<0.05),RAGE、COL-Ⅳ和iNOS蛋白的表达量升高(P<0.05);而治疗组小鼠病理损伤及纤维化改变均有改善,定量指标得到好转。GLP可以改善DN小鼠,机制与抑制RAGE信号通路有关。The study investigated the effects of Ganoderma lucidum polysaccharide(GLP)on diabetic nephropathy(DN)in mice.After successfully establishing a DN mouse model,GLP intervention was administered.The fasting blood glucose and 24-hour urinary protein content of the mice were measured,and the levels of blood urea nitrogen(BUN)and serum creatinine(Scr)were determined.Eosin and Masson′s trichrome staining were used to observe the renal pathological morphology.Enzyme-linked immunosorbent assay was employed to measure the levels of tumor necrosis factor-alpha(TNF-α),interleukin-6(IL-6),and interleukin-10(IL-10).Western blot was utilized to detect the expression of receptor for advanced glycation end-products(RAGE),collagen type IV(COL-IV),and inducible nitric oxide synthase(iNOS).Mice in the DN group exhibited increased levels of fasting blood glucose,24-hour urinary protein,BUN,and Scr as well as elevated levels of TNF-αand IL-6 in renal tissue(P<0.05),and decreased levels of serum IL-10(P<0.05).The expression of RAGE,COL-IV,and iNOS proteins was also increased(P<0.05).In contrast,mice in the treatment group showed improvements in pathological damage and fibrosis,with quantitative indicators showing significant amelioration.GLP could ameliorate DN in mice,and the mechanism is associated with the inhibition of the RAGE signaling pathway.
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