α-actin-2

Ac-Ala-OH (N-Acetyl-L-alanine) 是鸟嘌呤核苷酸结合蛋白G(I) G(S) G(O) γ -2亚基、髓鞘碱性蛋白、GTP-结合核蛋白 Ran、原肌球蛋白 α - 4链、HIV-1 Rev 结合蛋白2、Xaa-Pro 二肽酶、胸腺酶 β -10、肌动蛋白样蛋白3、丙氨酸转氨酶、丝氨酸 苏氨酸蛋白磷酸酶PP1 - β催化亚基、10 kda 热休克蛋白(线粒体)、钙调蛋白和 β -1-syntrophin 的底物。

alpha-Cyperone (α-Cyperone) 与 IL-6, Cox-2, Cdc42, Nck-2, Rac1 的表达下调相关,从而能够抑制炎症反应。

The growth factors, platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) play major roles in enhanced smooth muscle cells growth in rodent blood vessels after vascular injury. Tyrosine kinase inhibition has been shown to be effective in blocking tyrosine phosphorylation at the PDGF and bFGF receptors in cultured fibroblast and vascular smooth muscle cells which in turn inhibits their proliferation[1]. CGP 53716 is a specific PDGFR tyrosine kinase inhibitor on SMC (smooth muscle cell) proliferation and migration in vitro and in neointimal formationin vivo[3]. CGP 53716 inhibited serum-induced cell growth in RASMC (rat aortic smooth muscle cells). And it completely blocked PDGF-BB tyrosine receptor autophosphorylation in RASMC and 3T3 cells, PDGF-BB-induced phosphorylation of mitogen-activated protein kinase at 1 μM in RASMC and inhibited PDGF-BB-induced c-Fos protein expression at 1 μM in RASMC; consistent with inhibition of PDGF-BB-induced DNA synthesis. Further, CGP 53716 inhibited PDGF-BB-, bFGF- and EGF-induced DNA synthesis in a concentration-dependent manner in each cell line. And it showed a 2- to 4-fold selectivity for PDGF-BB-stimulated DNA synthesis over bFGF or EGF in RASMC or 3T3 cells[1]. CGP 53716 inhibited dose dependently tyrosine phosphorylation of both the known PDGFRs: the PDGFR-α and PDGFR-β. After rat carotid artery ballooning injuryin vivo, the migration of alpha-actin-positive cells on the luminal side of internal elastic lamina was decreased with 50 mg kg day of CGP 53716 from 38 ± 10 (control group) to 4 ± 2. Intima media ratio was inhibited by 40% after 14 days in the CGP 53716-treated group (P=0.028) after rat aortic denudation[3].

Klotho衍生肽1（KP1）(56-87)是从人类Klotho蛋白质中衍生的肽，具有扰乱TGF-β信号传导的作用。它与TGF-β受体类型1（TGFBR2）和TGF-β受体类型2（TGFBR2；Kds分别为1.41和14.6µM）结合。KP1（10 µg/ml）的预孵育抑制TGF-β在NRK-49F大鼠成纤维细胞中诱导的纤维连接蛋白和α-平滑肌肌动蛋白（α-SMA）水平的增加。在体内，KP1（每天1 mg/kg）选择性地定位于受损的肾脏，并减少血清肌酐和血尿素氮水平，这些是肾功能的标志物，同时也减少了小鼠单侧输尿管阻塞（UUO）和单侧缺血-再灌注损伤诱导的肾脏纤维化模型中的肾纤维化。