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番茄红素通过自噬调节在胰腺炎中的修复潜力。

The Remedial Potential of Lycopene in Pancreatitis through Regulation of Autophagy.

机构信息

Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul 03722, Korea.

出版信息

Int J Mol Sci. 2020 Aug 12;21(16):5775. doi: 10.3390/ijms21165775.

DOI:10.3390/ijms21165775
PMID:32806545
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7460830/
Abstract

Autophagy is an evolutionarily conserved process that degrades damaged organelles and recycles macromolecules to support cell survival. However, in certain disease states, dysregulated autophagy can play an important role in cell death. In pancreatitis, the accumulation of autophagic vacuoles and damaged mitochondria and premature activation of trypsinogen are shown in pancreatic acinar cells (PACs), which are the hallmarks of impaired autophagy. Oxidative stress mediates inflammatory signaling and cytokine expression in PACs, and it also causes mitochondrial dysfunction and dysregulated autophagy. Thus, oxidative stress may be a mediator for autophagic impairment in pancreatitis. Lycopene is a natural pigment that contributes to the red color of fruits and vegetables. Due to its antioxidant activity, it inhibited oxidative stress-induced expression of cytokines in experimental models of acute pancreatitis. Lycopene reduces cell death through the activation of 5'-AMP-activated protein kinase-dependent autophagy in certain cells. Therefore, lycopene may ameliorate pancreatitis by preventing oxidative stress-induced impairment of autophagy and/or by directly activating autophagy in PACs.

摘要

自噬是一种进化上保守的过程,可降解受损的细胞器并回收大分子以支持细胞存活。然而,在某些疾病状态下,失调的自噬可能在细胞死亡中起重要作用。在胰腺炎中,胰腺腺泡细胞 (PACs) 中积聚自噬空泡和受损的线粒体以及胰蛋白酶原的过早激活是自噬受损的标志。氧化应激介导 PACs 中的炎症信号和细胞因子表达,还导致线粒体功能障碍和自噬失调。因此,氧化应激可能是胰腺炎中自噬受损的介质。番茄红素是一种天然色素,使水果和蔬菜呈现红色。由于其抗氧化活性,它抑制了急性胰腺炎实验模型中氧化应激诱导的细胞因子表达。番茄红素通过激活某些细胞中的 5'-AMP 激活蛋白激酶依赖性自噬来减少细胞死亡。因此,番茄红素可能通过防止氧化应激诱导的自噬受损和/或通过直接激活 PACs 中的自噬来改善胰腺炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58e3/7460830/be97b1fc81b9/ijms-21-05775-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58e3/7460830/be97b1fc81b9/ijms-21-05775-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58e3/7460830/be97b1fc81b9/ijms-21-05775-g001.jpg

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