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作 者:成细华[1] 程莉娟[1] 绕春梅 唐元[2] 罗文娟[2] 尹婷[2] 喻嵘[1]
机构地区:[1]湖南中医药大学中西医结合基础湖南省重点学科,国家重点学科国家中医药管理局病理生理实验室和中医诊断学湖南省重点实验室,湖南410208 [2]湖南中医药大学
出 处:《北京中医药大学学报》2014年第12期812-815,I0007,共5页Journal of Beijing University of Traditional Chinese Medicine
基 金:国家自然科学基金项目(No.81102593,81273753);中国博士后科学基金项目(No.20110491258)
摘 要:目的探讨滋阴益气活血解毒中药含药血清对脂肪酸孵育Hep G2细胞中固醇调节元件结合蛋白-1c(SREBP-1c)和脂肪酸合成酶(FAS)表达的影响。方法 Hep G2细胞分为对照组、模型组、15%含药血清组;对照组和模型组用正常大鼠血清DMEM培养,15%含药血清组用15%含药血清DMEM培养,模型组、15%含药血清组同时加0.5 mmol/L混合脂肪酸(油酸∶棕榈酸=2∶1);油红O染色法检测细胞内脂质沉积,RT-PCR检测Hep G2细胞SREBP-1c和FAS mRNA表达,免疫组化检测Hep G2细胞SREBP-1c和FAS蛋白表达。结果 15%含药血清能减少模型细胞脂质沉积,降低模型细胞SREBP-1c和FAS的mRNA及蛋白表达,差异具有统计学意义(P<0.01)。结论滋阴益气活血解毒中药含药血清能够调节SREBP-1c和FAS表达,改善混合脂肪酸诱导的Hep G2细胞脂肪性变。Objective To investigate the effects of serum with yin-enriching,qi-replenishing,and bloodactivating Chinese medicine on the expressions of SREBP-1 c and FAS in steatotic HepG2 cells.Methods HepG2 cells were randomly divided into the control group,model group,and 15% medicated serum group.The control group and model group were cultured with normal rat serum DMEM while the 15% medicated serum group was given 15% medicated serum DMEM.Moreover,mixed fatty acids (oleic acid,hexadecanoic acid =2:1) (0.5 mmol/L) were added to the model group and the 15% medicated serum group.The lipid content in HepG2 cells was analyzed by using oil red O staining method.The mRNA expressions of SREBP-1c and FAS were detected by using reverse transcription-polymerase chain reaction (RT-PCR).The protein expressions of SREBP-1c and FAS were detected by using the immunohistochemistry technique.Results Serum with yin-enriching,qi-replenishing,blood-activating Chinese medicine induced a decrease in lipid accumulation in 15% medicated serum group and it also down-regulated the mRNA and protein expressions of SREBP-1c and FAS in the model group.Statistically significant difference was observed (P < 0.01).Conclusion The serum medicated with yin-enriching,qi-replenishing,and blood-activating Chinese medicine improves the excessive lipid accumulation in steatotic HepG2 cells by down-regulating the expressions of SREBP-1 c and FAS.
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