
@Article{biocell.2021.015261,
AUTHOR = {YIBIN RUAN, ZHONGMING XIE, QIONG LIU, LIXIAO ZHANG, XIKUI HAN, XIAOYAN LIAO, JIAN LIU, FENGGUANG GAO},
TITLE = {Nicotine and menthol independently exert neuroprotective effects against cisplatin- or amyloid- toxicity by upregulating Bcl-xl via JNK activation in SH-SY5Y cells},
JOURNAL = {BIOCELL},
VOLUME = {45},
YEAR = {2021},
NUMBER = {4},
PAGES = {1059--1067},
URL = {http://www.techscience.com/biocell/v45n4/42366},
ISSN = {1667-5746},
ABSTRACT = {Nicotine and menthol, agonists of nicotinic acetylcholine receptor (nAChR) and transient receptor potential
melastatin type 8 (TRPM8), serve important roles in the prevention of cell death-involved neurodegenerative diseases.
However, the potential synergistic effects of nicotine and menthol on anti-apoptotic ability are still uncertain. In the
present study, the potential synergistic effects of nicotine and menthol on cisplatin or amyloid β<sub>1-42</sub> induced cell
model of the neurodegenerative diseases were explored by assessing cell viability, TNF-α expression, caspase-3
activation, and the collapse of mitochondrial membrane potential in human SH-SY5Y neuroblastoma cells. Statistical
significance was tested using Student’s <i>t</i>-test or one-way ANOVA with <i>post hoc</i> Newman-Keuls test. The results
showed that: Firstly, SH-SY5Y cell viability was obviously increased by the treatments with nicotine and menthol.
Secondly, nicotine and menthol independently alleviated cisplatin or amyloid β<sub>1-42</sub> induced TNF-α up-regulation.
Thirdly, nicotine and menthol abrogated the effect of cisplatin and amyloid β<sub>25-35</sub> on caspase-3 activation.
Interestingly, the effect of cisplatin and amyloid β<sub>1-42</sub> on the collapse of mitochondrial membrane potential was
efficiently attenuated by nicotine and menthol treatments. Most importantly, the inhibition of c-jun kinase (JNK)
activation abolished the effect of cisplatin, and amyloid β<sub>1-42</sub> stimulated Bcl-xl expression. All these findings indicate
that nicotine and menthol independently exert neuroprotective effects by upregulating Bcl-xl <i>via</i> JNK activation.
Nicotine and menthol augmented Bcl-xl expression and JNK phosphorylation, and thus they are potential therapeutic
targets for altering the progress of neurodegenerative diseases.},
DOI = {10.32604/biocell.2021.015261}
}



