【摘要】 目的探讨肉桂醛在高血糖诱导的心肌纤维化进程中的保护作用以及可能的调控信号通路等机制。方法高糖饲养持续喂养乳鼠12周并肉桂醛处理心肌纤维化细胞48小时(对照组无肉桂醛处理),麻醉处死乳鼠取出心脏,并进行病理包埋切片、HE染色,CCK8法检测细胞的增殖情况;分离乳鼠心肌成纤维细胞,分别在含5.6 m M正常葡糖糖和25 m M高葡萄糖培养基培养24h后,用流式Annexin-FITC/PI双染法检测细胞凋亡;设计miR-1252特异性引物,运用q PCR检测其在各组处理心肌成纤维细胞的表达水平。结果低糖培养条件下,心肌细胞排列整齐,结构完整;高糖培养破坏细胞形态,结构组织紊乱;流式Annexin-FITC/PI双染法检测细胞凋亡,发现高糖能显著诱导心肌成纤维细胞的凋亡,而CA能抑制心肌成纤维细胞的凋亡。miR-1252在高糖诱导的心肌成纤维细胞的表达水平要显著低于正常组和CA组。结论肉桂醛可以改善高糖毒性对乳鼠心肌细胞的损伤,抑制心肌成纤维细胞的凋亡,可能是通过刺激miR-1252的表达的机制改善心肌纤维化。更多还原

【Abstract】 Objective To investigate the protective effect of cinnamaldehyde on hyperglycemia induced myocardial fibrosis and the possible regulatory signaling pathways. Methods The rats were fed with high glucose for 12 weeks,and cinnamaldehyde treated with cinnamaldehyde for 48 hours( the control group without cinnamaldehyde treatment). The rats were killed and the heart was taken out by the anesthesia,and the pathology was embedded and stained with HE. The proliferation of the cells was detected by CCK8.The rat myocardial fibroblasts were isolated and cultured for 24 h containing 5. 6 m M normal glucose and 25 m M high glucose medium,and apoptosis was detected by flow Annexin-FITC/PI double staining. MiR-1252 specific primers were designed,and q PCR was used to detect the expression level of myocardial fibroblasts in each group. Results Under the condition of low sugar culture,the myocardial cells were arranged orderly and the structure was intact. The apoptosis of the cells was detected by flow Annexin-FITC/PI double staining. It was found that high glucose could induce apoptosis of myocardial fibroblasts,and CA could inhibit the apoptosis of myocardial fibroblasts. The expression level of miR-1252 in high glucose induced cardiac fibroblasts was significantly lower than that in normal group and CA group. Conclusions Cinnamaldehyde can improve the damage of hyperglycemia to neonatal rat cardiomyocytes and inhibit the apoptosis of myocardial fibroblasts. The myocardial fibrosis can be improved by stimulating the expression of miR-1252.更多还原