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褪黑素通过内质网应激诱导抗炎作用在急性胰腺炎中发挥保护作用。

Melatonin Induces Anti-Inflammatory Effects to Play a Protective Role via Endoplasmic Reticulum Stress in Acute Pancreatitis.

作者信息

Chen Yina, Zhang Jie, Zhao Qian, Chen Qinfen, Sun Yangjie, Jin Yin, Wu Jiansheng

机构信息

Department of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

出版信息

Cell Physiol Biochem. 2016;40(5):1094-1104. doi: 10.1159/000453164. Epub 2016 Dec 14.

Abstract

BACKGROUND/AIMS: Melatonin, which is mainly secreted by the pineal gland and released into blood, has anti-inflammatory properties in acute pancreatitis. Many studies show that melatonin can relieve inflammation in taurocholate-induced acute pancreatitis. However, the mechanisms of its anti-inflammatory effects are still undefined, especially the relationship between melatonin and endoplasmic reticulum stress. We explored the anti-inflammatory activity of melatonin in AR42J and rat models.

METHODS

The CCK-8 assay was used to assess effects of melatonin on AR42J cell viability. Inflammatory degree and the expressions of endoplasmic reticulum stress related molecules were examined by quantitative RT-PCR and western blotting. The degree of inflammation in the tissue was also accessed by pathological grading. Finally, we used the western blotting method to verify apoptosis and autophagy.

RESULTS

Endoplasmic reticulum stress was obviously activated in early stage inflammation in AR42J and rat models. Melatonin could induce anti-inflammatory effects via endoplasmic reticulum stress. Melatonin significantly inhibited inflammatory cytokines and the expression of ERS-related molecules. Finally, it played a protective role by promoting apoptosis and autophagy of the cells, which were damaged in the process of inflammatory reaction.

CONCLUSION

Melatonin induces anti-inflammatory effects via endoplasmic reticulum stress in acute pancreatitis to play a protective role.

摘要

背景/目的:褪黑素主要由松果体分泌并释放到血液中,在急性胰腺炎中具有抗炎特性。许多研究表明,褪黑素可减轻牛磺胆酸盐诱导的急性胰腺炎中的炎症。然而,其抗炎作用的机制仍不明确,尤其是褪黑素与内质网应激之间的关系。我们在AR42J和大鼠模型中探究了褪黑素的抗炎活性。

方法

采用CCK-8法评估褪黑素对AR42J细胞活力的影响。通过定量RT-PCR和蛋白质印迹法检测炎症程度及内质网应激相关分子的表达。还通过病理分级评估组织中的炎症程度。最后,我们用蛋白质印迹法验证细胞凋亡和自噬。

结果

在AR42J和大鼠模型的早期炎症中,内质网应激明显被激活。褪黑素可通过内质网应激诱导抗炎作用。褪黑素显著抑制炎性细胞因子和内质网应激相关分子的表达。最后,它通过促进在炎症反应过程中受损细胞的凋亡和自噬发挥保护作用。

结论

褪黑素在急性胰腺炎中通过内质网应激诱导抗炎作用以发挥保护作用。

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