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[酸性稳定的羧基末端片段(AcSDKP)对培养的大鼠心脏成纤维细胞中胶原蛋白合成与降解的作用]

[Role of AcSDKP on collagen synthesis and degradation in cultured rat cardiac fibroblast].

作者信息

Yang Fang, Zhu Xi-ling, Wang Li-ping, Song Xu-dong, Wang Rui-min, Li Zhi-guo, Luo Ling, Hu Wan-mi, Ma Wen-dong, Pei Xin, Zhang Li-juan, Li Qi-jia

机构信息

Experimental and Research Center, North China Coal Medical College, Tangshan 063000, China.

出版信息

Zhonghua Xin Xue Guan Bing Za Zhi. 2006 Sep;34(9):843-6.

Abstract

OBJECTIVE

To investigate the role of AcSDKP on collagen synthesis and degradation in cultured rat cardiac fibroblasts.

METHODS

Neonatal rat cardiac fibroblasts were isolated and stimulated by PDGF. The cell proliferation was observed by (3)H-TdR incorporation assay. The synthesis of collagen was measured by (3)H-proline incorporation assay. The expression of type I and type III collagen and MMP-1 protein were measured by Western blot. The MMP-2 and MMP-9 activity was evaluated with zymography assay.

RESULTS

PDGF stimulated cardiac fibroblasts proliferation with increased collagen synthesis and type I and type III collagen protein expressions as well as MMP-2 and MMP-9 activities and MMP-1 expression. AcSDKP inhibited cardiac fibroblasts proliferation induced by PDGF and reduced collagen synthesis and type I and type III collagen protein expression. AcSDKP also further up-regulated MMP-2 and MMP-9 activities and MMP-1 expression in cardiac fibroblasts induced by PDGF.

CONCLUSION

AcSDKP inhibited proliferation and collagen synthesis and up-regulated matrix metalloproteinases activity or expression induced by PDGF, which was possibly related with the effect of AcSDKP anti-fibrosis.

摘要

目的

研究N-乙酰-S-天门冬氨酰-L-半胱氨酸(AcSDKP)对培养的大鼠心脏成纤维细胞胶原合成与降解的作用。

方法

分离新生大鼠心脏成纤维细胞并给予血小板源性生长因子(PDGF)刺激。通过³H-胸腺嘧啶核苷掺入法观察细胞增殖。通过³H-脯氨酸掺入法测定胶原合成。采用蛋白质免疫印迹法检测Ⅰ型和Ⅲ型胶原以及基质金属蛋白酶-1(MMP-1)蛋白的表达。用酶谱分析法评估基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶-9(MMP-9)的活性。

结果

PDGF刺激心脏成纤维细胞增殖,同时胶原合成增加,Ⅰ型和Ⅲ型胶原蛋白表达以及MMP-2和MMP-9活性及MMP-1表达升高。AcSDKP抑制PDGF诱导的心脏成纤维细胞增殖,并减少胶原合成以及Ⅰ型和Ⅲ型胶原蛋白表达。AcSDKP还进一步上调PDGF诱导的心脏成纤维细胞中MMP-2和MMP-9活性以及MMP-1表达。

结论

AcSDKP抑制增殖和胶原合成,并上调PDGF诱导的基质金属蛋白酶活性或表达,这可能与AcSDKP的抗纤维化作用有关。

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