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作 者:程梅[1] 李保应[1] 王茜[1] 许玲[1] 高海青[1]
机构地区:[1]山东大学齐鲁医院老年病科 山东省心血管蛋白质组学重点实验室,济南250012
出 处:《中华老年医学杂志》2011年第11期958-961,共4页Chinese Journal of Geriatrics
基 金:国家自然科学基金(30873145);山东省自然科学基金资助项目(Y2008C100)
摘 要:目的探讨葡萄籽原花青素(GSPE)对糖尿病大鼠心肌糖基化终末产物受体(RAGE)、核转录因子κB(NF-κB)和结缔组织生长因子(CTGF)的影响。方法将链脲佐菌素诱导的糖尿病大鼠30只随机分为两组,糖尿病未治疗组(糖尿病1组)和糖尿病GSPE治疗组(糖尿病2组,每日给予GSPE2 50mg/kg灌胃)各15只;正常大鼠20只随机分为正常对照组(对照1组)和正常GSPE治疗组(对照2组,每日给予GSPE 250mg/kg灌胃)各10只,24周后采血检测空腹血糖(FBG)、糖基化终末产物(AGEs),免疫组织化学染色和Western blot测定心肌NFKB蛋白的表达,并应用Western blot测定各组心肌RAGE和CTGF的蛋白表达变化。结果糖尿病1组FBG、血清AGEs含量较对照1组显著升高(P〈0.05),经GSPE治疗后,血清AGEs含量显著降低(P〈0.05),而FBG降低差异无统计学意义;糖尿病1组心肌组织RAGE、NF—κB和CTGF蛋白表达较对照1组显著升高(P〈0.05),GSPE能够显著抑制RAGE、NF—κB和CTGF蛋白表达。结论GSPE对糖尿病心肌病具有保护作用,其可能机制与抑制糖尿病大鼠AGEs-RAGE、NF—κB和CTGF的表达有关。Objective To investigate the effects of grape seed proanthocyanidin extracts (GSPE) on advanced glycation end product receptor (RAGE), NF -κB and connective tissue growth factor (CTGF) in the myocardium of diabetic rats. Methods Total 30 streptozotocin (STZ) induced diabetic rats were randomly divided into 2 groups: diabetic group (DM1, n= 15) and GSPE (250 mg/ kg, i.g) treated diabetic group (DM2, n 15). Another two control groups: normalrats(C1, n=10) and normal rats treated with GSPE (250 mg/kg, i. g) (C2 group, n=10) were also observed. After 24 weeks, blood was collected to measure fasting plasma glucose (FBG) and RAGE. The protein expression of NF -κB was determined in myocardial tissue by immunohistochemical staining and Western blot. The protein expressions of RAGE and CTGF were measured by Western blot. Results The levels of FBG and RAGE were significantly higher in diabetic rats than in control rats (P〈 0.05). After GSPE treatment, RAGE level significantly reduced (P〈0.05), but FBG had no change in diabetic rats. The protein expressions of RAGE, NF -κB and CTGF in the myocardial tissue of diabetic rats had marked increase compared with control rats (P 〈 0.05), however, their levels significantly reduced after GSPE treatment (P〈0.05). Conclusions GSPE may protect diabetic rats against cardiomyopathy, possibly by decreasing the protein expressions of RAGE, NF -κB and CTGF.
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