Protective and Therapeutic Properties of Obestatin in Experimental Models of Acute Pancreatitis

J. Bukowczan, T. Golabek
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Abstract

Acute pancreatitis (AP) still remains associated with high mortality rates reaching as high as 30% despite substantial improvements in the management of the disease [1,2]. This is due to complex disease aetiology, its diverse clinical course, as well as, the lack of targeted treatment owning to the poor understanding of its pathogenesis. A number of histological mechanisms have been associated with AP and are responsible for permanent morphological and structural changes of the gland in the course of severe AP [3]. The article "Pretreatment with obestatin reduces the severity of ischemia/reperfusion-induced acute pancreatitis in rats" provides fascinating data how administration of obestatin inhibits the development of ischemia/ reperfusion-induced AP [4]. Authors’ conclusions, together with previous findings, suggest that protective effect of obestatin in the pancreas is universal and independent of the primary cause of acute pancreatitis. The observations are in agreement that different initial causes can damage pancreas through same mechanisms or even through different mechanisms, which, however, share same end-point biochemical and histological markers (very uncommon in human biology), as obestatin probably expresses its protective effect, according to the results, through controlling all these biochemical and histopathological parameters which definitely express a specific mechanism of pancreatic damage (oxidative stress). The study prompts a question about what should be an acceptable possible way of obestatin to fail to express its protection in case of ischemia/ reperfusion-induced AP. The phenomenon of obestatin protection seems to be oxidative stressand dose-dependent. Accordingly, the reason for the statistically insignificant blood flow improvement although statistically significant oxidative stress scavenging, remains unknown. Relative changes in the expression of these results do not alter, however, the core issue of this important question.
肥胖抑素对急性胰腺炎实验模型的保护和治疗作用
急性胰腺炎(AP)仍然与高达30%的高死亡率相关,尽管该病的治疗有了实质性的改善[1,2]。这是由于该病的病因复杂,临床过程多样,以及由于对其发病机制了解不足而缺乏针对性的治疗。许多组织学机制与AP相关,并在严重AP过程中导致腺体的永久性形态和结构变化[3]。“用肥胖抑制素预处理降低大鼠缺血/再灌注诱导的急性胰腺炎的严重程度”这篇文章提供了肥胖抑制素如何抑制缺血/再灌注诱导的AP发展的有趣数据[4]。作者的结论,连同先前的发现,表明肥胖抑制素对胰腺的保护作用是普遍的,与急性胰腺炎的主要原因无关。观察结果一致认为,不同的初始原因可以通过相同的机制甚至不同的机制损害胰腺,然而,它们具有相同的终点生化和组织学标记(在人类生物学中非常罕见),因为根据结果,肥胖抑制素可能通过控制所有这些生化和组织病理学参数来表达其保护作用,这些参数明确表达了胰腺损伤的特定机制(氧化应激)。该研究提出了一个问题,即在缺血/再灌注诱导的AP中,肥胖抑制素不能表达其保护作用的可接受的可能方式是什么。肥胖抑制素的保护现象似乎是氧化应激和剂量依赖性的。因此,尽管统计上有显著的氧化应激清除,但统计上不显著的血流量改善的原因仍然未知。然而,这些结果表达的相对变化并没有改变这个重要问题的核心问题。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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