N-Acetyl-Ser-Asp-Lys-Pro

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

乙酰 Ser-Asp-Lys-Pro 通过胸腺肽 β4 的酶促处理在骨髓细胞中形成。它抑制多能造血干细胞进入细胞周期的 S 期，并防止小鼠中的 Ara-C 致死。N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) 是 N 端的特异性底物ACE 抑制剂治疗期间增加 5 倍。 AcSDKP抑制分离的心脏成纤维细胞的增殖（P<0.05），但显着刺激血管平滑肌细胞的增殖。

Acetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?Flow cytometry of rat cardiac fibroblasts treated with AcSDKP showed significant inhibition of the progression of cells from G0/G1 phase to S phase of the cell cycle.?In cardiac fibroblasts transfected with a Smad-sensitive luciferase reporter construct, AcSDKP decreased luciferase activity by 55+/-9.7% (P=0.01).?Moreover, phosphorylation and nuclear translocation of Smad2 was decreased in cardiac fibroblasts treated with AcSDKP.?To conclude, AcSDKP inhibits the growth of cardiac fibroblasts and also inhibits TGFbeta1-stimulated phosphorylation of Smad2.?Because AcSDKP increases substantially during ACE inhibitor therapy, this suggests a novel pathway independent of angiotensin II, by which ACE inhibitors can inhibit cardiac fibrosis.

N-Acetyl-Ser-Asp-Lys-Pro is degraded specifically by ACE, and its plasma level rises substantially during ACE inhibitor therapy. Flow cytometry of rat cardiac fibroblasts treated with N-Acetyl-Ser-Asp-Lys-Pro shows significant inhibition of the progression of cells from G0/G1 phase to S phase of the cell cycle. Moreover, phosphorylation and nuclear translocation of Smad2 is decreased in cardiac fibroblasts treated with N-Acetyl-Ser-Asp-Lys-Pro. N-acetyl-seryl-aspartyl-lysyl-proline appears to exert this function by blocking the action of a stem cell-specific proliferation stimulator and acts selectively on quiescent progenitors. N-Acetyl-Ser-Asp-Lys-Pro inhibits collagenase expression and activation is associated with increased expression of TIMP-1 and TIMP-2. N-Acetyl-Ser-Asp-Lys-Pro normalizes the IL-1β-mediated increase in MMP-2 and MMP-9 activities and MMP-13 expression.

N-Acetyl-Ser-Asp-Lys-Pro prevents hypertension-induced inflammatory cell infiltration, collagen deposition, nephrin downregulation and albuminuria, which could lead to renoprotection in hypertensive mice.

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Endocrinology/Hormones

RAAS

ACE

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127103-11-1

487.5

C20H33N5O9

>98% (HPLC)

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O=C([C@@H]1N(C([C@H](NC([C@@H](NC([C@H](NC(C)=O)CO)=O)CC(O)=O)=O)CCCCN)=O)CCC1)O

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(-20℃)

With Ice Pack

≥ 2 years