论文部分内容阅读
目的:探讨肌肽对高糖环境下心肌成纤维细胞中胶原生成的影响及作用机制。方法:原代培养心肌成纤维细胞,将细胞分为正常糖组(NG,5.5mmol/L glucose)、高糖组(HG,25mmol/L glucose)、高糖+10mmol/L肌肽组、高糖+20mmol/L肌肽组、高糖+40mmol/L肌肽组、高糖+SB组(HG+10μmol/L SB203580)、高糖+PD组(HG+10μmol/L PD98059)。ELISA检测胶原Ⅰ、Ⅲ的含量,Western blot检测TGF-β1、p-p38 MAPK和p-ERK(1/2)等蛋白的表达。结果:与正常糖组相比,高糖组中胶原Ⅰ和胶原Ⅲ含量增加(P<0.01);TGF-β1、p-p38和p-ERK等表达增加(P<0.01);与高糖组相比,高糖+肌肽组中胶原Ⅰ、Ⅲ、TGF-β1、p-p38、和p-ERK等均降低(P<0.05);高糖+SB组和高糖+PD组中胶原Ⅰ、Ⅲ表达减少(P<0.05)。结论:肌肽对心肌成纤维细胞中胶原生成具有抑制作用,且通过MAPK通路实现。
Objective: To investigate the effect of carnosine on collagen production in cardiac fibroblasts under high glucose conditions and its mechanism. Methods: Primary cultured cardiac fibroblasts were divided into normal glucose group (NG, 5.5mmol / L glucose), high glucose group (HG, 25mmol / L glucose), high glucose + 10mmol / L carnosine group, +20 mmol / L carnosine group, high glucose +40 mmol / L carnosine group, high glucose + SB group (HG +10 μmol / L SB203580) and high glucose + PD group (HG +10 μmol / L PD98059). The contents of collagen Ⅰ and Ⅲ were detected by ELISA. The expressions of TGF-β1, p-p38 MAPK and p-ERK (1/2) were detected by Western blot. Results: Compared with normal glucose group, the content of collagen Ⅰ and collagen Ⅲ in high glucose group increased (P <0.01), the expression of TGF-β1, p-p38 and p-ERK increased Collagen Ⅰ, Ⅲ, TGF-β1, p-p38 and p-ERK in high glucose + carnosine group were significantly decreased (P <0.05) Ⅲ decreased (P <0.05). CONCLUSION: Carnosine inhibits collagen production in cardiac fibroblasts and is mediated by the MAPK pathway.