首页> 外文期刊>American Journal of Physiology >Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage
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Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage

机译:高血压诱导的靶器官损伤中N-乙酰基-SC-Lys-Pro的新型抗炎机制

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摘要

Ac-SDKP is an endogenous peptide released from its precursor (thymosin-p4) by proline oligopeptidase (9, 12). Ac-SDKP is a natural inhibitor of pluripotent hematopoietic stem cell proliferation (5) and is normally found in human plasma and circulating monocyte cells (2). Early on, Ac-SDKP was shown to originate from bone marrow (19), but it has recently been shown that in mice both Ac-SDKP and its precursor are ubiquitously distributed in tissues including the lung, kidney, and heart (31). Ac-SDKP is mainly hydrolyzed by angiotensin converting enzyme (ACE), and ACE inhibitors (ACEi) prevent its hydrolysis and raise its concentration in plasma four- to fivefold (2).
机译:AC-SDKP是通过脯氨酸寡肽(9,12)从其前体(胸腺蛋白-P4)释放的内源性肽。 AC-SDKP是多能造血干细胞增殖(5)的天然抑制剂,通常在人血浆和循环单核细胞细胞(2)中。 早期,AC-SDKP显示出源自骨髓(19),但最近已显示在小鼠中,ac-SDKP及其前体在包括肺,肾和心脏(31)的组织中普遍存花出。 AC-SDKP主要由血管紧张素转换酶(ACE)水解,ACE抑制剂(ACEI)防止其水解并将其浓度升高到血浆四至五倍(2)中。

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