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作 者:王芳[1] 陈筱菲[2] 陈国荣[1] 李旭升[1] 雷康福[3] 毛孙忠[3]
机构地区:[1]温州医学院附属第一医院病理科 [2]温州医学院附属第一医院检验科,浙江温州325027 [3]温州医学院生物化学教研室,浙江温州325027
出 处:《中国病理生理杂志》2006年第10期2036-2039,共4页Chinese Journal of Pathophysiology
基 金:浙江省教委资助项目(No.Y2000674);温州市科技局项目(No.Y2003A014)
摘 要:目的:研究银杏叶提取物(EGb)对2型糖尿病大鼠脂代谢及巨噬细胞功能的影响。方法:SD大鼠分4组:正常对照组、高脂组、糖尿病组、EGb治疗组,治疗结束取血测血糖、血脂、血胰岛素并分别灌取4组大鼠腹腔及肺泡巨噬细胞,测定巨噬细胞内超氧化物歧化酶(SOD)、一氧化氮(NO)及丙二醛(MDA)的水平,并用RT-PCR方法测定大鼠肺泡巨噬细胞内CD36、PPARγ的基因表达水平。结果:糖尿病大鼠血糖、血胰岛素、总胆固醇(TC)、总甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)升高,经EGb治疗后,血糖、血胰岛素、TC、TG、LDL-C明显降低;糖尿病大鼠腹腔及肺泡巨噬细胞内SOD活性下降、NO及MDA含量增高,经EGb治疗后,SOD活性升高、NO2-/NO3-及MDA含量下降;糖尿病大鼠肺泡巨噬细胞CD36基因表达升高,PPARγ基因表达升高,经EGb治疗后,CD36基因表达继续升高但无显著差异、PPARγ基因表达继续升高。结论:EGb对糖尿病大鼠巨噬细胞脂质过氧化有较好的拮抗作用,并能降低一氧化氮含量,从而改善糖尿病时巨噬细胞功能;EGb可提高2型糖尿病大鼠肺泡巨噬细胞CD36、PPARγ基因的表达水平,这可能是其降血脂和改善胰岛素抵抗的机制之一。AIM : To study effect of extract of ginkgo biloba (EGb) on the lipid metabolism and the function of macrophages from diabetic rats. METHODS : Sprague - Dauley rats were divided into four groups : normal control group, high -fat group, diabetic group and EGb treatment group. At the end of experiment, the rats were sacrificed, the blood glucose, blood insulin and serum lipid were measured. The activity of superoxide dismutase ( SOD), content of malondialdehyde (MDA), nitric oxide (NO) in alveolar macrophages (AM) and peritoneal macrophages (PM) were assayed. In addition, peroxisome proliferator activated receptor γ ( PPARγ), CD36 mRNA expression in AM was measured by RT - PCR. RESULTS: The concentration of the blood glucose, blood insulin and total cholesterol (TC) , total triglycerides (TG), low- density lipoprotein - cholesterol (LDL- C) in blood increased significantly in type 2 diabetic group. The supplement of EGb decreased blood glucose, blood insulin and TC, TG, LDL - C levels. The activity of SOD decreased, while the content of NO, MDA increased in the diabetic macrophages, the activity of SOD became increased, but the content of NO and MDA decreased in EGb - treated group. The mRNA expression level of CD36 and PPARγ in alveolar macrophages from diabetic group increased, while expression level of CD36 and PPARγ mRNA in EGb treated rats continued to rise. CONCLUSIONS : EGb corrected insulin resistance and ameliorated disturbance of lipid metabolism caused by type2 diabetes in rats. Adjustment of PPARγ and CD36 mRNA expression of as well as reduction of lipid peroxidation and NO level may be involved in this process.
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