黄芪多糖对脂多糖诱导大鼠心肌细胞肥大的保护作用

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。

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

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(P<0.01).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(P<0.05).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(P<0.01).Conclusion APS does have a good protection on cultured cardiac myocytes hypertrophy and its mechanism may be related to the inhibition of [Ca2+]i.