黄芪多糖对脂多糖诱导大鼠心肌细胞肥大的保护作用  

Protection of astragalus polysaccharide on lipopolysaccharide-induced cardiac myocytes hypertrophy of rats

作　　者：周振华[1] 王洪新[1] 赵素玲[1] 喻晓春[2] 张晶[1] 宋莹[1] 

机构地区：[1]辽宁医学院分子生物学与新药开发重点实验室,辽宁锦州121001 [2]中国中医科学院实验中心,北京100700

出　　处：《中草药》2012年第3期524-528,共5页Chinese Traditional and Herbal Drugs

基　　金：国家自然科学基金资助项目(30973898/C190702)

摘　　要：目的研究黄芪多糖对脂多糖(LPS)诱导的大鼠心肌细胞肥大的保护作用。方法新生1～2 d的SD大鼠心肌细胞培养48 h后,设对照组,模型组,黄芪多糖低、中、高质量浓度(1、10、100 mg/L)组。计算机图像分析系统测量细胞体积;RT-PCR法检测心房利钠多肽(ANP)mRNA的表达;ELISA法检测细胞肿瘤坏死因子-α(TNF-α)的量;采用Fluo-3/Am荧光染色剂负载细胞,在激光共聚焦显微镜下测定细胞内钙离子浓度([Ca2+]i)的瞬间变化。结果与对照组相比,LPS 1 mg/L可使心肌细胞体积显著增大,ANP mRNA的表达显著增强,细胞分泌TNF-α蛋白的量显著增加,心肌细胞内[Ca2+]i瞬间峰值增大(P<0.01)。与模型组相比,黄芪多糖1、10、100 mg/L预先给药均可抑制心肌细胞体积增大;细胞产生的TNF-α显著减少,ANP mRNA的表达不同程度地减少(P<0.05),其中10、100 mg/L组这两项指标可恢复到对照组的水平(P>0.05);黄芪多糖10 mg/L可拮抗LPS对正常心肌细胞内[Ca2+]i瞬间变化幅度增大的作用(P<0.01)。结论黄芪多糖对LPS诱导的乳鼠心肌细胞肥大有良好的保护作用,其机制可能与抑制TNF-α的产生、降低[Ca2+]i有关。Objective To investigate the protective effect of astragalus polysaccharide（APS） on lipopolysaccharide（LPS）-induced cardiac myocytes hypertrophy of rats and its mechanism.Methods Cardiac myocytes of 1—2 d neonatal SD rats were cultured 48 h in vitro,and divided into control,model（LPS 1 mg/L） group,APS low-,middle-,and high-（1,10,and 100 mg/L） groups.The cardiomyocyte volume was assayed by computer photograph analysis;atrial natriuretic peptide（ANP） mRNA expression was measured by RT-PCR;and tumor necrosis factor-α（TNF-α） level was determined by ELISA.The transient peak change of intracellular calcium concentration（[Ca2＋]i） was measured by using Fluo-3/Am fluorescent dye load cell under laser confocal microscope.Results Compared with control group,LPS 1 mg/L could make the volume of myocardial cells,ANP mRNA expression,the release of TNF-α protein,and [Ca2＋]itransient peak increase significantly（P0.01）.Compared with the LPS model group,APS pre-administrated at the concentrations of 1,10,and 100 mg/L could inhibit myocardial cell volume increase,while cells of TNF-α were significantly reduced,ANP mRNA expression decreased in varying degrees（P0.05）.APS 10 and 100 mg/L groups could be restored to normal levels of the control group（P 0.05） and APS 10 mg/L could antagonize transient changes in amplitude increase of [Ca2＋]i in normal cardiac myocytes（P0.01）.Conclusion APS does have a good protection on cultured cardiac myocytes hypertrophy and its mechanism may be related to the inhibition of [Ca2＋]i.

关 键 词：黄芪多糖 脂多糖 心肌细胞肥大 肿瘤坏死因子-α 钙离子 心房利钠多肽 

分 类 号：R282.710.5[医药卫生—中药学] R972.9[医药卫生—中医学]