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胃饥饿素、瘦素和褪黑素在急性胰腺炎中的激素保护作用。

Hormonal protection in acute pancreatitis by ghrelin, leptin and melatonin.

作者信息

Jaworek Jolanta, Konturek Stanisław Jan

机构信息

Jolanta Jaworek, Department of Medical Physiology, Faculty of Health Sciences, Jagiellonian University Collegium Medicum, 31-125 Kraków, Poland.

出版信息

World J Gastroenterol. 2014 Dec 7;20(45):16902-12. doi: 10.3748/wjg.v20.i45.16902.

Abstract

Acute pancreatitis is a nonbacterial disease of the pancreas. The severe form of this ailment is characterized by high mortality. Whether acute pancreatitis develops as the severe type or resolves depends on the intensity of the inflammatory process which is counteracted by the recruitment of innate defense mechanisms. It has been shown that the hormones ghrelin, leptin and melatonin are able to modulate the immune function of the organism and to protect the pancreas against inflammatory damage. Experimental studies have demonstrated that the application of these substances prior to the induction of acute pancreatitis significantly attenuated the intensity of the inflammation and reduced pancreatic tissue damage. The pancreatic protective mechanisms of the above hormones have been related to the mobilization of non-specific immune defense, to the inhibition of nuclear factor kappa B and modulation of cytokine production, to the stimulation of heat shock proteins and changes of apoptotic processes in the acinar cells, as well as to the activation of antioxidant system of the pancreatic tissue. The protective effect of ghrelin seems to be indirect and perhaps dependent on the release of growth hormone and insulin-like growth factor 1. Leptin and ghrelin, but not melatonin, employ sensory nerves in their beneficial action on acute pancreatitis. It is very likely that ghrelin, leptin and melatonin could be implicated in the natural protection of the pancreatic gland against inflammatory damage because the blood levels of these substances increase in the initial phase of pancreatic inflammation. The above hormones could be a part of the innate resistance system which might remove noxious factors and could suppress or attenuate the inflammatory process in the pancreas.

摘要

急性胰腺炎是胰腺的一种非细菌性疾病。这种疾病的严重形式具有高死亡率的特征。急性胰腺炎是发展为重症型还是痊愈,取决于炎症过程的强度,而炎症过程会受到固有防御机制激活的对抗。研究表明,胃饥饿素、瘦素和褪黑素能够调节机体的免疫功能,并保护胰腺免受炎症损伤。实验研究表明,在诱导急性胰腺炎之前应用这些物质可显著减轻炎症强度并减少胰腺组织损伤。上述激素的胰腺保护机制与非特异性免疫防御的动员、核因子κB的抑制和细胞因子产生的调节、热休克蛋白的刺激以及腺泡细胞凋亡过程的变化有关,还与胰腺组织抗氧化系统的激活有关。胃饥饿素的保护作用似乎是间接的,可能依赖于生长激素和胰岛素样生长因子1的释放。瘦素和胃饥饿素而非褪黑素,在对急性胰腺炎的有益作用中利用感觉神经。很可能胃饥饿素、瘦素和褪黑素参与了胰腺对炎症损伤的天然保护,因为在胰腺炎症的初始阶段这些物质的血液水平会升高。上述激素可能是固有抵抗系统的一部分,该系统可能清除有害因子并抑制或减轻胰腺中的炎症过程。

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