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[细胞外信号调节激酶1/2在N-乙酰丝氨酰-天冬氨酰-赖氨酰-脯氨酸抑制血小板衍生生长因子诱导的大鼠肺成纤维细胞增殖及胶原合成中的作用]

[Role of extracellular signal-regulated kinase 1/2 on inhibition of N-acetyl-seryl-aspartyl-lysyl-proline on proliferation and collagen synthesis of cultured rat pulmonary fibroblasts induced by platelet-derived growth factor].

作者信息

Wu Kun-Fei, Fang Yang, Li Dan-Dan, Zhang Li-Juan, Li Qian, Wang Rui-Min

机构信息

North China Coal Medical College, Tangshan 063000, China.

出版信息

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2009 Jul;27(7):385-9.

Abstract

OBJECTIVE

To investigate the role of extracellular signal-regulated kinase 1/2 on the inhibition of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on the proliferation and collagen synthesis of cultured rat pulmonary fibroblasts induced by platelet-derived growth factor (PDGF).

METHODS

Pulmonary fibroblasts were prepared from lungs of neonatal Wistar rats as described previously. Cells were divided into 4 groups: (1) control group (0.4% FBS group); (2) PDGF (10 ng/ml) stimulated group; (3) PD98059+PDGF group (25 micromol/L PD98059+10 ng/ml PDGF); (4) AcSDKP+PDGF group (10(-8) mol/L AcSDKP+10 ng/ml PDGF). All experiments were performed in the fourth passages. Metabolic activity of fibroblasts was observed by MTT, and expressions of type I and type III collagen were measured by immunocytochemistry and western blot. Expressions of phospho-ERK1/2 and ERK1/2 were detected by western blot.

RESULTS

Compared with control group, exposure of pulmonary fibroblasts to 10 ng/ml PDGF increased cell metabolic activity, expression of type I and type III collagen and phosphorylation of ERK1/2. 25 micromol/L PD98059 and AcSDKP both could inhibit the metabolic activity of pulmonary fibroblasts, type I and type III collagen synthesis and phosphorylation of ERK1/ 2 induced by PDGF, with significant differences (P < 0.05). AcSDKP+PDGF group compared with PDGF stimulated group, metabolic activity of pulmonary fibroblasts decreased to 77.4%. Immunocytochemistry result showed that in AcSDKP+PDGF group, expressions of type I and type III collagen decreased to 69.3% and 67.2% compared with those of PDGF stimulated group. Western blot result showed that in AcSDKP+PDGF group, expressions of type I and type III collagen decreased to 92.4% and 78.0%, phospho-ERK1/2 decreased to 83.5% compared with those of PDGF stimulated group, with significant differences (P < 0.05).

CONCLUSION

ERK1/2 plays an important role in the inhibition of AcSDKP on the proliferation and collagen synthesis of cultured rat pulmonary fibroblasts induced by PDGF.

摘要

目的

探讨细胞外信号调节激酶1/2在N - 乙酰 - 丝氨酰 - 天冬氨酰 - 赖氨酰 - 脯氨酸(AcSDKP)抑制血小板衍生生长因子(PDGF)诱导的大鼠肺成纤维细胞增殖及胶原合成中的作用。

方法

按照先前描述的方法从新生Wistar大鼠肺中制备肺成纤维细胞。细胞分为4组:(1)对照组(0.4%胎牛血清组);(2)PDGF(10 ng/ml)刺激组;(3)PD98059 + PDGF组(25 μmol/L PD98059 + 10 ng/ml PDGF);(4)AcSDKP + PDGF组(10⁻⁸ mol/L AcSDKP + 10 ng/ml PDGF)。所有实验均在第四代进行。通过MTT观察成纤维细胞的代谢活性,通过免疫细胞化学和蛋白质印迹法检测Ⅰ型和Ⅲ型胶原的表达。通过蛋白质印迹法检测磷酸化ERK1/2和ERK1/2的表达。

结果

与对照组相比,肺成纤维细胞暴露于10 ng/ml PDGF可增加细胞代谢活性、Ⅰ型和Ⅲ型胶原表达以及ERK1/2磷酸化。25 μmol/L PD98059和AcSDKP均可抑制PDGF诱导的肺成纤维细胞代谢活性、Ⅰ型和Ⅲ型胶原合成以及ERK1/2磷酸化,差异有统计学意义(P < 0.05)。AcSDKP + PDGF组与PDGF刺激组相比,肺成纤维细胞代谢活性降至77.4%。免疫细胞化学结果显示,AcSDKP + PDGF组中,Ⅰ型和Ⅲ型胶原表达与PDGF刺激组相比分别降至69.3%和67.2%。蛋白质印迹结果显示,AcSDKP + PDGF组中,Ⅰ型和Ⅲ型胶原表达与PDGF刺激组相比分别降至92.4%和78.0%,磷酸化ERK1/2降至83.5%,差异有统计学意义(P < 0.05)。

结论

ERK1/2在AcSDKP抑制PDGF诱导的大鼠肺成纤维细胞增殖及胶原合成中起重要作用。

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