Nicotine therapeutic benefits: Difference between revisions

Line 721:

**Citation: Lee, M.‐Y., Chen, L. and Toborek, M. (2009), Nicotine attenuates iNOS expression and contributes to neuroprotection in a compressive model of spinal cord injury. J. Neurosci. Res., 87: 937-947.doi.org/10.1002/jnr.21901

***Acknowledgement: This work was supported in part by the Philip Morris External Research Program and the Kentucky Science and Engineering Foundation.

===2008 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693390/ Neuronal Nicotinic Alpha7 Receptors Modulate Inflammatory Cytokine Production in the Skin Following Ultraviolet Radiation]===

*Animal study

*Cytokine responses to UV in mice administered chronic oral nicotine, a nAChR agonist, were reduced... These results demonstrate that nAChRα7 can participate in modulating a local pro-inflammatory response in the absence of parasympathetic innervation.

**Citation: Osborne-Hereford AV, Rogers SW, Gahring LC. Neuronal nicotinic alpha7 receptors modulate inflammatory cytokine production in the skin following ultraviolet radiation. J Neuroimmunol. 2008 Jan;193(1-2):130-9. doi: 10.1016/j.jneuroim.2007.10.029. PMID: 18077004; PMCID: PMC2693390.

***Acknowledgement: These studies were funded by NIH grants DA015148 and DA018930 (LCG), PO1 HL72903 (LCG, SWR) and the Browning Foundation of Utah.

===2006 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809735/ Nicotine inhibits the production of proinflammatory mediators in human monocytes by suppression of I-κB phosphorylation and nuclear factor-κB transcriptional activity through nicotinic acetylcholine receptor α7]===

@@ Line 721: / Line 721: @@
 **Citation: Lee, M.‐Y., Chen, L. and Toborek, M. (2009), Nicotine attenuates iNOS expression and contributes to neuroprotection in a compressive model of spinal cord injury. J. Neurosci. Res., 87: 937-947.doi.org/10.1002/jnr.21901
 ***Acknowledgement: This work was supported in part by the Philip Morris External Research Program and the Kentucky Science and Engineering Foundation.
+===2008 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693390/ Neuronal Nicotinic Alpha7 Receptors Modulate Inflammatory Cytokine Production in the Skin Following Ultraviolet Radiation]===
+*Animal study
+*Cytokine responses to UV in mice administered chronic oral nicotine, a nAChR agonist, were reduced... These results demonstrate that nAChRα7 can participate in modulating a local pro-inflammatory response in the absence of parasympathetic innervation.
+**Citation: Osborne-Hereford AV, Rogers SW, Gahring LC. Neuronal nicotinic alpha7 receptors modulate inflammatory cytokine production in the skin following ultraviolet radiation. J Neuroimmunol. 2008 Jan;193(1-2):130-9. doi: 10.1016/j.jneuroim.2007.10.029. PMID: 18077004; PMCID: PMC2693390.
+***Acknowledgement: These studies were funded by NIH grants DA015148 and DA018930 (LCG), PO1 HL72903 (LCG, SWR) and the Browning Foundation of Utah.
 ===2006 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809735/ Nicotine inhibits the production of proinflammatory mediators in human monocytes by suppression of I-κB phosphorylation and nuclear factor-κB transcriptional activity through nicotinic acetylcholine receptor α7]===