Vol.45, No.4, 2021, pp.1059-1067, doi:10.32604/biocell.2021.015261
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ARTICLE
Nicotine and menthol independently exert neuroprotective effects against cisplatin- or amyloid- toxicity by upregulating Bcl-xl via JNK activation in SH-SY5Y cells
  • YIBIN RUAN1, ZHONGMING XIE2, QIONG LIU2, LIXIAO ZHANG2, XIKUI HAN2, XIAOYAN LIAO2, JIAN LIU1,*, FENGGUANG GAO2,*
1 Technology Center, China Tobacco Guizhou Industrial Co., Ltd., Guiyang, 550003, China
2 Department of Basic Medical Sciences, School of Medicine, Xiamen University, Xiamen, 361102, China
* Address correspondence to: Jian Liu, ; Fengguang Gao,
Received 04 December 2020; Accepted 08 February 2021; Issue published 22 April 2021
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 β1-42 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 t-test or one-way ANOVA with post hoc 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 β1-42 induced TNF-α up-regulation. Thirdly, nicotine and menthol abrogated the effect of cisplatin and amyloid β25-35 on caspase-3 activation. Interestingly, the effect of cisplatin and amyloid β1-42 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 β1-42 stimulated Bcl-xl expression. All these findings indicate that nicotine and menthol independently exert neuroprotective effects by upregulating Bcl-xl via 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.
Keywords
Nicotine, Menthol, Apoptosis, Mitochondrial membrane potential, Tumor necrosis factor-alpha
Cite This Article
RUAN, Y., XIE, Z., LIU, Q., ZHANG, L., HAN, X. et al. (2021). Nicotine and menthol independently exert neuroprotective effects against cisplatin- or amyloid- toxicity by upregulating Bcl-xl via JNK activation in SH-SY5Y cells. BIOCELL, 45(4), 1059–1067.
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