Mimouni S, Raffaitin C, Corcuff J-B
Service de médecine nucléaire, CHU Bordeaux.
Ann Biol Clin (Paris). 2006 Jan-Feb;64(1):11-6.
The tetra-peptide Acetyl-Ser-Asp-Lys-Pro (Ac-SDKP) generated by the cleavage of thymosine beta4 inhibits the proliferation of hematopoietic stem cells and the proliferation and secretion of fibroblasts in the myocardium and the glomeruli. The clinical administration of Ac-SDKP has been proposed and partially investigated. The peptide could protect hematopoietic stem cells during anti-neoplastic treatments leaving cancerous cells unprotected. As it opposes the effects of TGFbeta it could prevent fibrosis after myocardial infarcts and glomeruli fibrosis during the natural course of diabetic nephropathy. However, until now the expected benefits of such a treatment are based on an indirect consideration. Indeed, the degradation of Ac-SDKP is due to the action of the angiotensin-converting enzyme. Interestingly, the blocking of this enzyme both improves the above-mentioned fibrosis and increases the plasma levels of Ac-SDKP. Should the therapeutic effects prove solid, and therapeutic levels be established assaying Ac-SDKP could be an interesting marker of therapeutic efficiency.
胸腺素β4裂解产生的四肽乙酰丝氨酸-天冬氨酸-赖氨酸-脯氨酸（Ac-SDKP）可抑制造血干细胞的增殖以及心肌和成纤维细胞在肾小球中的增殖和分泌。有人提出并对Ac-SDKP的临床应用进行了部分研究。该肽可在抗肿瘤治疗期间保护造血干细胞，而癌细胞则得不到保护。由于它能对抗转化生长因子β的作用，因此可以预防心肌梗死后的纤维化以及糖尿病肾病自然病程中的肾小球纤维化。然而，到目前为止，这种治疗预期的益处是基于间接的考虑。实际上，Ac-SDKP的降解是由于血管紧张素转换酶的作用。有趣的是，抑制这种酶既能改善上述纤维化，又能提高Ac-SDKP的血浆水平。如果治疗效果得到证实，并确定了治疗水平，那么检测Ac-SDKP可能是一个有趣的治疗效果标志物。
