Protective Effect of Zeaxanthin on Tunicamycin-Induced Cell Cycle Arrest, Autophagy and Apoptosis of SH-SY5Y Cells

被引：0
|
作者：
Zhang L. [1 ]
Li M. [1 ]
Shang Y. [1 ]
Liu Y. [1 ]
Huang H. [1 ]
Lao F. [1 ]
机构：
[1] Beijing Key Laboratory of Bioactive Substances and Functional Foods, Institute of Functional Factors and Brain Science, Beijing Union University, Beijing
来源：
Shipin Kexue/Food Science | 2022年 / 43卷 / 07期
基金：
英国惠康基金;
关键词：
Apoptosis; Autophagy; Cell cycle; SH-SY5Y cells; Zeaxanthin;
D O I：
10.7506/spkx1002-6630-20210325-318
中图分类号：
学科分类号：
摘要：
Objective: To investigate the effect of co-treatment with zeaxanthin (Zea) and tunicamycin (TM) on the viability, cell cycle, autophagy and apoptosis of SH-SY5Y cells. Methods: The cells were divided into four groups: blank control (without drug treatment), Zea (5 μmol/L), TM-induced injury (5 μg/mL) and Zea (5 μmol/L) + TM (5 μg/mL). The methylthiazol tetrazolium (MTT) method was used to evaluate the survival rate of SH-SY5Y cells to determine the drug co-treatment time for further experiments; flow cytometry was used to determine the change of cell cycle; Western blot was used to determine the expression of autophagy-related proteins such as Beclin1, Beclin1-C and microtubule-associated protein 1 light chain 3B (LC3B), and apoptosis-related protein B-cell lymphoma 2 (BCL2). Results: Zea treatment (5 μmol/L)reduced the inhibitory effect of TM on the survival rate of SH-SY5Y cells. Compared to the injury group, a significant difference in the survival rate of SH-SY5Y cells was observed for the combined treatment group at 36 (P < 0.01) and 48 h(P < 0.05). In addition, compared to the blank control group, TM treatment displayed a significant difference in the survival rate of SH-SY5Y cells at 24, 36, and 48 h (P < 0.01). Compared to the blank group, TM treatment significantly increased the number of G0/G1 phase cells in the cell cycle (P < 0.01) and the expression of LC3B (P < 0.01), Beclin1 (P < 0.05)and Beclin1-C (P < 0.05), and significantly reduced the number of G2/M phase cells (P < 0.01) and the expression level of anti-apoptotic protein BCL2 (P < 0.01). The combined treatment alleviated the changes caused by TM, and significantly increased BCL2 protein expression compared to the injury group (P < 0.05). Conclusion: Zea can significantly extenuate TM-induced cell cycle G1 arrest, autophagy and apoptosis of SH-SY5Y cells, and its underlying mechanism is related to the modulatory of Zea on cell survival, cell cycle distribution, and the expression of autophagy and apoptosis-related proteins. © 2022, China Food Publishing Company. All right reserved.
引用
收藏
页码：112 / 119
页数：7
相关论文
共 33 条
  • [1] MCKHANN G M, KNOPMAN D S, CHERTKOW H, Et al., The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease, Alzheimer's & Dementia, 7, 3, pp. 263-269, (2011)
  • [2] LOPEZ J A S, GONZALEZ H M, LEGER G C., Alzheimer's disease, Handbook of Clinical Neurology, 167, pp. 231-255, (2019)
  • [3] MUELLER K D, HERMANN B, MECOLLARI J, Et al., Connected speech and language in mild cognitive impairment and Alzheimer's disease: a review of picture description tasks, Journal of Clinical and Experimental Neuropsychology, 40, 9, pp. 917-939, (2018)
  • [4] PAMPLONA F A, PANDOLFO P, DUARTE F S, Et al., Altered emotionality leads to increased pain tolerance in amyloid beta(Abeta1-40) peptide-treated mice, Behavioural Brain Research, 212, 1, pp. 96-102, (2010)
  • [5] VERMUNT L, SIKKES S A M, VAN DEN HOUT A, Et al., Duration of preclinical, prodromal, and dementia stages of Alzheimer's disease in relation to age, sex, and APOE genotype, Alzheimer's &Dementia, 15, 7, pp. 888-898, (2019)
  • [6] LONG J M, HOLTZMAN D M., Alzheimer disease: an update on pathobiology and treatment strategies, Cell, 179, 2, pp. 312-339, (2019)
  • [7] GAO H, YAN P, ZHANG S, Et al., Chronic alpha-linolenic acid treatment alleviates age-associated neuropathology: roles of PERK/eIF2α signaling pathway[J], Brain, Behavior, and Immunity, 57, pp. 314-325, (2016)
  • [8] ZHANG M, HAN N, JIANG Y, Et al., EGFR confers radioresistance in human oropharyngeal carcinoma by activating endoplasmic reticulum stress signaling PERK-eIF2α-GRP94 and IRE1α-XBP1-GRP78, Cancer Medicine, 7, 12, pp. 6234-6246, (2018)
  • [9] CHENG T L, CHEN P S, LI R H, Et al., Induction of apurinic endonuclease 1 overexpression by endoplasmic reticulum stress in hepatoma cells, International Journal of Molecular Sciences, 15, 7, pp. 12442-12457, (2014)
  • [10] JIAN L, LU Y, LU S, Et al., Chemical chaperone 4-phenylbutyric acid protects H9c2 cardiomyocytes from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis, Molecular Medicine Reports, 13, 5, pp. 4386-4392, (2016)
1234