Nicotine therapeutic benefits: Difference between revisions
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='''Cancer / Cancer Treatments'''=    | ='''Cancer / Cancer Treatments'''=    | ||
===2021 [https://www.mdpi.com/1660-3397/19/2/118 α-Conotoxins and α-Cobratoxin Promote, while Lipoxygenase and Cyclooxygenase Inhibitors Suppress the Proliferation of Glioma C6 Cells]===  | |||
*Animal Study  | |||
*We tested the effects of nicotine, which is an agonist for all nAChRs with the exception of α9 subtype for which it is antagonist. At concentrations of 0.001–0.1µL/mL (6.1 µM–0.61 mM), nicotine exerted no effect on the proliferative activity of glioma C6 cells and the loss of viability was 1–4% (Figure S2). Analysis by light microscopy showed that nicotine at concentrations of 1 µL/mL (6.1 mM) and higher induced morphological changes like cell rounding up and loss of processes followed by surface detachment (Figure 3). Despite these changes, we investigated the effect of nicotine at a concentration of 1 μL/mL (6.1 mM) on the proliferation and viability of C6 cells. At this nicotine concentration, inhibition of proliferation was observed, which after 72 h led to a decrease in the number of cells by more than two times; the viability was also reduced (Figure S2). However, it should be taken into account that the reason for such a strong decrease in the concentration of cells may be their detachment from the surface and, as a consequence, the cessation of division. We tested acetylcholine at concentrations ranging from 2 µM to 2 mM with incubation times of 24, 48 and 72 h. No effects of acetylcholine were observed.  | |||
**Citation: Terpinskaya, T. I., Osipov, A. V., Kryukova, E. V., Kudryavtsev, D. S., Kopylova, N. V., Yanchanka, T. L., Palukoshka, A. F., Gondarenko, E. A., Zhmak, M. N., Tsetlin, V. I., & Utkin, Y. N. (2021). α-Conotoxins and α-Cobratoxin Promote, while Lipoxygenase and Cyclooxygenase Inhibitors Suppress the Proliferation of Glioma C6 Cells. Marine Drugs, 19(2), 118. https://doi.org/10.3390/md19020118  | |||
***Acknowledgement: This work was supported by the Belarusian Republican Foundation for Fundamental Research, project number M20R-254, and the Russian Foundation for Basic Research, project number 20-54-00033.  | |||
===2020 [https://www.sciencedirect.com/science/article/abs/pii/S001448272030416X?via%3Dihub Nicotine inhibits MAPK signaling and spheroid invasion in ovarian cancer cells]===    | ===2020 [https://www.sciencedirect.com/science/article/abs/pii/S001448272030416X?via%3Dihub Nicotine inhibits MAPK signaling and spheroid invasion in ovarian cancer cells]===    | ||
*Nicotine inhibits ovarian cancer cell ERK and p38 [[Special:MyLanguage/Abbreviations|'''MAPK''']] signaling.  | *Nicotine inhibits ovarian cancer cell ERK and p38 [[Special:MyLanguage/Abbreviations|'''MAPK''']] signaling.  | ||
*Nicotine inhibits ovarian cancer proliferation and spheroid invasion.  | *Nicotine inhibits ovarian cancer proliferation and spheroid invasion.  | ||
*[https://sci-hub.se/10.1016/j.yexcr.2020.112167 PDF Version]  | *[https://sci-hub.se/10.1016/j.yexcr.2020.112167 PDF Version]  | ||
*Citation: Sarah J. Harmych, Jay Kumar, Mesa E. Bouni, Deborah N. Chadee, Nicotine inhibits MAPK signaling and spheroid invasion in ovarian cancer cells, Experimental Cell Research, Volume 394, Issue 1, 2020, 112167, ISSN 0014-4827, doi: 10.1016/j.yexcr.2020.112167.  | **Citation: Sarah J. Harmych, Jay Kumar, Mesa E. Bouni, Deborah N. Chadee, Nicotine inhibits MAPK signaling and spheroid invasion in ovarian cancer cells, Experimental Cell Research, Volume 394, Issue 1, 2020, 112167, ISSN 0014-4827, doi: 10.1016/j.yexcr.2020.112167.  | ||
*Acknowledgements: This work was supported by the National Institutes of Health [R15 CA199164] and [R15 CA241898] to D.N.C.    | ***Acknowledgements: This work was supported by the National Institutes of Health [R15 CA199164] and [R15 CA241898] to D.N.C.    | ||
===2013 [https://www.sciencedirect.com/science/article/abs/pii/S0014299913003270?via%3Dihub Nicotine is a pain reliever in trauma- and chemotherapy-induced neuropathy models]===    | ===2013 [https://www.sciencedirect.com/science/article/abs/pii/S0014299913003270?via%3Dihub Nicotine is a pain reliever in trauma- and chemotherapy-induced neuropathy models]===    | ||
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*Intraperitoneal nicotine administration controls neuropathic pain evoked by traumatic or toxic nervous system alterations. These results support the [[Special:MyLanguage/Abbreviations|'''nAChR''']] modulation as a possible therapeutic approach to the complex, undertreated chemotherapy-induced neuropathies.    | *Intraperitoneal nicotine administration controls neuropathic pain evoked by traumatic or toxic nervous system alterations. These results support the [[Special:MyLanguage/Abbreviations|'''nAChR''']] modulation as a possible therapeutic approach to the complex, undertreated chemotherapy-induced neuropathies.    | ||
*[https://sci-hub.st/https://doi.org/10.1016/j.ejphar.2013.04.022 PDF Version]  | *[https://sci-hub.st/https://doi.org/10.1016/j.ejphar.2013.04.022 PDF Version]  | ||
*Citation: Lorenzo Di Cesare Mannelli, Matteo Zanardelli, Carla Ghelardini, Nicotine is a pain reliever in trauma- and chemotherapy-induced neuropathy models, European Journal of Pharmacology, Volume 711, Issues 1–3, 2013, Pages 87-94, ISSN 0014-2999, doi: 10.1016/j.ejphar.2013.04.022.  | **Citation: Lorenzo Di Cesare Mannelli, Matteo Zanardelli, Carla Ghelardini, Nicotine is a pain reliever in trauma- and chemotherapy-induced neuropathy models, European Journal of Pharmacology, Volume 711, Issues 1–3, 2013, Pages 87-94, ISSN 0014-2999, doi: 10.1016/j.ejphar.2013.04.022.  | ||
*Acknowledgements: This work was supported by the Italian Ministry of Instruction, University and Research.  | ***Acknowledgements: This work was supported by the Italian Ministry of Instruction, University and Research.  | ||
='''Cannabis / THC'''=    | ='''Cannabis / THC'''=    | ||