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目的探讨细胞外信号调节激酶1/2(ERK1/2)及C-Jun氨基末端激酶(JNK)通路在N-乙酰基-丝氨酰-天门冬酰-赖氨酰-脯氨酸(AcSDKP)抑制血小板源性生长因子(PDGF)诱导的大鼠心脏成纤维细胞增殖和胶原蛋白表达中的作用。方法将新生Wistar大鼠心脏成纤维细胞分为对照组(A组)、10ng/ml PDGF刺激组(B组)、10-9 mol/L AcSDKP+10ng/ml PDGF干预组(C组)、25μmol/L PD98059+10ng/ml PDGF干预组(D组)和10nmol/L SP600125+10ng/ml PDGF干预组(E组)。MTT法检测心脏成纤维细胞代谢活性的变化,Western blot法检测大鼠心脏成纤维细胞中ERK1/2、JNK及磷酸化-ERK1/2、磷酸化-JNK蛋白表达和Ⅰ型、Ⅲ型胶原蛋白的表达。结果与A组相比,B组心脏成纤维细胞代谢活性、Ⅰ型及Ⅲ型胶原蛋白表达、磷酸化-ERK1/2及磷酸化-JNK蛋白表达均增强(P<0.05);而C、D、E组能明显逆转B组上述各观察指标的增加过程(P<0.05)。结论 AcSDKP能够通过阻断PDGF介导的ERK1/2及JNK通路的激活,进而抑制大鼠心脏成纤维细胞增殖和胶原蛋白表达。
Objective To investigate the role of ERK1 / 2 and C-Jun N-terminal kinase (JNK) pathways in N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) Inhibit platelet-derived growth factor (PDGF) -induced rat cardiac fibroblast proliferation and collagen expression. Methods Newborn Wistar rat cardiac fibroblasts were divided into control group (group A), 10ng / ml PDGF stimulation group (group B), 10-9mol / L AcSDKP + 10ng / ml PDGF intervention group (group C) / L PD98059 + 10ng / ml PDGF intervention group (D group) and 10nmol / L SP600125 + 10ng / ml PDGF intervention group (E group). The changes of metabolic activity of cardiac fibroblasts were detected by MTT assay. The expressions of ERK1 / 2, JNK, phospho-ERK1 / 2 and phospho-JNK in rat cardiac fibroblasts and expressions of type I and type III collagen expression. Results Compared with group A, the metabolic activity, the expression of type Ⅰ and type Ⅲ collagen, the expression of phosphorylated-ERK1 / 2 and phosphorylated-JNK in group B were significantly increased (P <0.05), while those in group C and D , E group can significantly reverse the increase of each of the above-mentioned indicators in group B (P <0.05). Conclusion AcSDKP can inhibit the proliferation of rat cardiac fibroblasts and the expression of collagen by blocking the activation of ERK1 / 2 and JNK pathway induced by PDGF.