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Protective effect of nicotine on tunicamycin-induced apoptosis of PC12h cells |
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| Authors: | Utsumi Takahiro Shimoke Koji Kishi Soichiro Sasaya Harue Ikeuchi Toshihiko Nakayama Hitoshi |
| Institution: | aLaboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University, 3-3-35 Yamate-cho, Suita, Osaka 564-8680, Japan bDepartment of Pharmacology, Nara Medical University, Kashihara, Nara 634-8521, Japan |
| Abstract: | Nicotine has been reported to have neuroprotective effects. The present study deals with the neuroprotective effect of nicotine on the tunicamycin-induced apoptosis of PC12h cells. Treatment of PC12h cells with tunicamycin causes endoplasmic reticulum stress leading to apoptosis. Nicotine dose-dependently prevented the tunicamycin-induced apoptosis. Hoechst 33258 staining demonstrated the protective effect of nicotine against tunicamycin-induced apoptosis. Treatment with nicotinic acetylcholine receptor (nAChR) and L-type voltage-sensitive calcium channel (L-VSCC) antagonists prevented the nicotine-induced protective effect. A phosphatidylinositol 3-kinase (PI3-K) inhibitor had no influence on the nicotine-induced neuroprotective effect. These results show that the neuroprotective effect of nicotine occurs through nAChRs including the alpha 7 subtype and L-VSCC in PC12h cells and not through the PI3-K/Akt pathway. |
| Keywords: | Acetylcholine receptor Endoplasmic reticulum stress Nicotine Nicotinic antagonist Phosphatidylinositol 3-kinase Tunicamycin |
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