Taxane-derived compounds protect SK-N-SH cells against oxidative stress injury induced by H2O2

被引:6
作者
Duan, Ruisheng [1 ]
Xing, Xing [1 ]
Qi, Yachao [1 ]
Yin, Nan [1 ]
Hao, Hongyu [1 ]
Chu, Hongshan [1 ]
Gao, Ya [1 ]
Wang, Weiping [2 ]
Lv, Peiyuan [1 ]
机构
[1] Hebei Gen Hosp, Dept Neurol, Shijiazhuang, Peoples R China
[2] Hebei Med Univ, Hosp 2, Dept Neurol, Shijiazhuang, Peoples R China
关键词
Taxane; oxidative stress; apoptosis; cell mitochondrial membrane potential; PEROXIDE-INDUCED APOPTOSIS; ENDOPLASMIC-RETICULUM; PC12; CELLS; RAT; NEURONS; METABOLISM; ACTIVATION; CALPAIN; DEATH; ROS;
D O I
10.1080/01616412.2017.1303579
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective: Discussed the protection of taxane-derived compounds, 7-deacetyl-taxine B and 5-cinnamoyloxy-taxin B, against oxidative stress injury. Methods: SK-N-SH cells were pretreated with 7-deacetyl-taxine B, 5-cinnamoyloxy-taxin B or DMSO (control) and then incubated with H2O2 for another 24 h. Cell viability was measured by MTT colorimetric assay. Apoptosis rate, reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were detected using flow cytometry assay. Ultrastructure was detected by Transmission electron microscope. Results: Taxane-derived compounds improved H2O2 mediated loss of cell viability in SK-NSH cell. Ultrastructure of control group cells showed nucleus shrinkage, dense aggregation of chromatin, appearance of apoptotic body and mitochondrial dilation. Treated group showed alleviation of mitochondrial dilation and chromatin margination, and reduction of apoptosis cells induced by H2O2. The apoptosis rate was decreased in treated group compared with control group. DCFH-DA staining showed that ROS were significantly decreased in cells treated with taxane-derived compounds compared with control group. Rhodamine123 staining showed that MMP was significantly decreased in cells treated with taxane-derived compounds compared with control group. Conclusion: The anti-oxidative stress and neuroprotective effect of taxane-derived compounds was verified here, wherein it could protect neurocytes from H2O2-induced oxidative stress injury.
引用
收藏
页码:632 / 639
页数:8
相关论文
共 33 条
[1]   Characterization of reactive oxygen species induced effects on human spermatozoa movement and energy metabolism [J].
Armstrong, JS ;
Rajasekaran, M ;
Chamulitrat, W ;
Gatti, P ;
Hellstrom, WJ ;
Sikka, SC .
FREE RADICAL BIOLOGY AND MEDICINE, 1999, 26 (7-8) :869-880
[2]   Oxidative stress in severe acute illness [J].
Bar-Or, David ;
Bar-Or, Raphael ;
Rael, Leonard T. ;
Brody, Edward N. .
REDOX BIOLOGY, 2015, 4 :340-345
[3]  
Bezard and Zhao, 2005, FREE RADICAL BIO MED, V39, P24
[4]   Apoptosis and interferons: Role of interferon-stimulated genes as mediators of apoptosis [J].
Chawla-Sarkar, M ;
Lindner, DJ ;
Liu, YF ;
Williams, B ;
Sen, GC ;
Silverman, RH ;
Borden, EC .
APOPTOSIS, 2003, 8 (03) :237-249
[5]   Mechanisms of ROS modulated cell survival during carcinogenesis [J].
Clerkin, J. S. ;
Naughton, R. ;
Quiney, C. ;
Cotter, T. G. .
CANCER LETTERS, 2008, 266 (01) :30-36
[6]   Effect of turmeric, turmerin and curcumin on H2O2-induced renal epithelial (LLC-PK1) cell injury [J].
Cohly, HHP ;
Taylor, A ;
Angel, MF ;
Salahudeen, AK .
FREE RADICAL BIOLOGY AND MEDICINE, 1998, 24 (01) :49-54
[7]   Traumatic Brain Injury: Oxidative Stress and Neuroprotection [J].
Cornelius, Carolin ;
Crupi, Rosalia ;
Calabrese, Vittorio ;
Graziano, Antonio ;
Milone, Pietro ;
Pennisi, Giovanni ;
Radak, Zsolt ;
Calabrese, Edward J. ;
Cuzzocrea, Salvatore .
ANTIOXIDANTS & REDOX SIGNALING, 2013, 19 (08) :836-853
[8]   Hsp27 binding to the 3′UTR of bim mRNA prevents neuronal death during oxidative stress-induced injury: a novel cytoprotective mechanism [J].
Davila, David ;
Jimenez-Mateos, Eva M. ;
Mooney, Claire M. ;
Velasco, Guillermo ;
Henshall, David C. ;
Prehn, Jochen H. M. .
MOLECULAR BIOLOGY OF THE CELL, 2014, 25 (21) :3413-3423
[9]  
[Duan Ruisheng 段瑞生], 2010, [天然产物研究与开发, Natural Product R & D], V22, P201
[10]   Mitochondrial enzymes and endoplasmic reticulum calcium stores as targets of oxidative stress in neurodegenerative diseases [J].
Gibson, GE ;
Huang, HM .
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 2004, 36 (04) :335-340