Wang Ting, Kong Xiang-Quan, Wang Wei-Hua
Department of Clinical Medicine, Wannan Medical College, Wuhu 241000, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2013 Mar;29(2):179-81, 192.
To investigate the effect of an anti-fibrotic tetra peptide Ac-SDKP on vascular fibrosis by regulating extracellular regulated protein kinase (ERK1/2) activity through Ang II.
Rat vascular adventitial fibroblasts were cultured in vitro. They were randomly divided into control group, Ang II (10(-6) mmol/L) group, Ang II and Ac-SDKP joint action group, PD98059 group. Type I, III collagen contents in adventitia fibroblasts were measured by RT-PCR and the expressions of matrix metalloproteinases (MMP-2) and transforming growth factor-beta1 (TGF-beta1) were determined by Western blot.
Ac-SDKP could reduced Ang II-induced expression of type I, III collagen secretion and TGF-beta1 at mRNA,and increase MMP-2 expression, PD98059 could inhibit the above effect.
The results suggested that Ac-SDKP could inhibit the formation and development of vascular fibrosis through blocking ERK1/2 pathway mediated by Ang II. Ac-SDKP therefore served as an antifibrotic factor in vascular fibrosis.
通过血管紧张素II(Ang II)调节细胞外调节蛋白激酶(ERK1/2)活性,探讨抗纤维化四肽Ac-SDKP对血管纤维化的影响。
体外培养大鼠血管外膜成纤维细胞。将其随机分为对照组、Ang II(10(-6) mmol/L)组、Ang II与Ac-SDKP联合作用组、PD98059组。采用RT-PCR检测外膜成纤维细胞中I、III型胶原含量,Western blot检测基质金属蛋白酶(MMP-2)和转化生长因子-β1(TGF-β1)的表达。
Ac-SDKP可降低Ang II诱导的I、III型胶原分泌及TGF-β1 mRNA表达,增加MMP-2表达,PD98059可抑制上述作用。
结果提示,Ac-SDKP可通过阻断Ang II介导的ERK1/2通路抑制血管纤维化的形成和发展。因此,Ac-SDKP在血管纤维化中作为一种抗纤维化因子发挥作用。