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枸杞糖肽对邻苯二甲酸二(2-乙基己基)酯诱导的肾和睾丸损伤的影响。

Effects of Lycium barbarum glycopeptide on renal and testicular injury induced by di(2-ethylhexyl) phthalate.

机构信息

Department of Nephrology, The First Affiliated Hospital of Jinan University, 613 Huangpu Avenue West, Guangzhou, 510630, Guangdong, China.

School of Traditional Chinese Medicine, Jinan University, Guangzhou, 510630, China.

出版信息

Cell Stress Chaperones. 2022 May;27(3):257-271. doi: 10.1007/s12192-022-01266-0. Epub 2022 Apr 1.

Abstract

Di(2-ethylhexyl) phthalate (DEHP) is a common environmental pollutant with renal and reproductive toxicity. Lycium barbarum glycopeptide (LbGp) is the main active component of Lycium barbarum, which can protect the kidney and promote reproduction. Autophagy and apoptosis are the regulatory mechanisms of cell adaptation to external stress. This study investigated whether DEHP and LbGp affect kidney and testis by regulating autophagy and apoptosis. DEHP induced apoptosis in human embryonic kidney-293 (HEK-293) cells and human kidney-2 (HK-2) cells, as well as glomerular enlargement, enhanced renal autophagy and inflammation, decreased testicular germ cells, and enhanced testicular autophagy. LbGp reduced apoptosis in HEK-293 cells and HK-2 cells, reduced glomerular enlargement and renal inflammation, enhanced renal autophagy, increased testicular germ cells, and alleviated testicular autophagy. These results suggested that DEHP induced inflammation to cause kidney injury, mildly enhanced renal autophagy, and also induced excessive autophagy, leading to testicular injury. LbGp reduced inflammation and appropriately enhanced autophagy to alleviate renal injury and also reduced excessive autophagy to alleviate testicular injury. Silent information regulator 1 (SIRT1)/forkhead box O3a (FoxO3a)-mediated autophagy and p38 mitogen-activated protein kinase (p38 MAPK)-mediated inflammation played important roles.

摘要

邻苯二甲酸二(2-乙基己基)酯(DEHP)是一种常见的环境污染物,具有肾毒性和生殖毒性。枸杞糖肽(LbGp)是枸杞的主要活性成分,能保护肾脏和促进生殖。自噬和细胞凋亡是细胞适应外部应激的调节机制。本研究探讨了 DEHP 和 LbGp 是否通过调节自噬和细胞凋亡来影响肾脏和睾丸。DEHP 诱导人胚肾-293(HEK-293)细胞和人肾-2(HK-2)细胞凋亡,导致肾小球肿大,增强肾脏自噬和炎症,减少睾丸生殖细胞,增强睾丸自噬。LbGp 减少 HEK-293 细胞和 HK-2 细胞的凋亡,减少肾小球肿大和肾脏炎症,增强肾脏自噬,增加睾丸生殖细胞,减轻睾丸自噬。这些结果表明,DEHP 诱导炎症导致肾脏损伤,轻度增强肾脏自噬,同时也诱导过度自噬,导致睾丸损伤。LbGp 减少炎症并适度增强自噬以减轻肾脏损伤,并减少过度自噬以减轻睾丸损伤。沉默信息调节因子 1(SIRT1)/叉头框 O3a(FoxO3a)介导的自噬和 p38 丝裂原激活蛋白激酶(p38 MAPK)介导的炎症发挥了重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59c7/9106773/abca1b6af66f/12192_2022_1266_Fig1_HTML.jpg

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