Nicotine therapeutic benefits: Difference between revisions

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**Citation: Abbaspour S, Fahanik-Babaei J, Adeli S, Hermann DM, Sardari M. Acute nicotine exposure attenuates neurological deficits, ischemic injury and brain inflammatory responses and restores hippocampal long-term potentiation in ischemic stroke followed by lipopolysaccharide-induced sepsis-like state. Exp Neurol. 2024 Sep 13;382:114946. doi: 10.1016/j.expneurol.2024.114946. Epub ahead of print. PMID: 39278587.

***Funding: None

===2014 [https://academic.oup.com/jid/article/209/10/1668/855517#78932729 Stimulation of the α7 nicotinic acetylcholine receptor protects against sepsis by inhibiting Toll-like receptor via phosphoinositide 3-kinase activation]===

*Animal study

*In conclusion, stimulation of α7nAChR by nicotine improves mortality rates and MODS during sepsis. This protective effect of nicotine can be associated with the inhibition of TLR4 overexpression through the PI3K/Akt signaling pathway. Although the therapeutic potential of nicotine is still limited by its nonspecific effects, this study may provide an impetus for further development of therapeutic strategies for modifying the cholinergic antiinflammatory pathway in the treatment of various inflammatory diseases.

**Citation: Kim TH, Kim SJ, Lee SM. Stimulation of the α7 nicotinic acetylcholine receptor protects against sepsis by inhibiting Toll-like receptor via phosphoinositide 3-kinase activation. J Infect Dis. 2014 May 15;209(10):1668-77. doi: 10.1093/infdis/jit669. Epub 2013 Dec 1. Erratum in: J Infect Dis. 2015 Mar 1;211(5):851. doi: 10.1093/infdis/jiu824. PMID: 24298024.

***Acknowledgement: This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, Information and Communication Technologies (ICT) and Future Planning (NRF-2013R1A1A3008145).

===2005 [https://academic.oup.com/jid/article/191/12/2138/842542 The Cholinergic Anti-Inflammatory Pathway Regulates the Host Response during Septic Peritonitis]===

@@ Line 1,233: / Line 1,233: @@
 **Citation: Abbaspour S, Fahanik-Babaei J, Adeli S, Hermann DM, Sardari M. Acute nicotine exposure attenuates neurological deficits, ischemic injury and brain inflammatory responses and restores hippocampal long-term potentiation in ischemic stroke followed by lipopolysaccharide-induced sepsis-like state. Exp Neurol. 2024 Sep 13;382:114946. doi: 10.1016/j.expneurol.2024.114946. Epub ahead of print. PMID: 39278587.
 ***Funding: None
+===2014 [https://academic.oup.com/jid/article/209/10/1668/855517#78932729 Stimulation of the α7 nicotinic acetylcholine receptor protects against sepsis by inhibiting Toll-like receptor via phosphoinositide 3-kinase activation]===
+*Animal study
+*In conclusion, stimulation of α7nAChR by nicotine improves mortality rates and MODS during sepsis. This protective effect of nicotine can be associated with the inhibition of TLR4 overexpression through the PI3K/Akt signaling pathway. Although the therapeutic potential of nicotine is still limited by its nonspecific effects, this study may provide an impetus for further development of therapeutic strategies for modifying the cholinergic antiinflammatory pathway in the treatment of various inflammatory diseases.
+**Citation: Kim TH, Kim SJ, Lee SM. Stimulation of the α7 nicotinic acetylcholine receptor protects against sepsis by inhibiting Toll-like receptor via phosphoinositide 3-kinase activation. J Infect Dis. 2014 May 15;209(10):1668-77. doi: 10.1093/infdis/jit669. Epub 2013 Dec 1. Erratum in: J Infect Dis. 2015 Mar 1;211(5):851. doi: 10.1093/infdis/jiu824. PMID: 24298024.
+***Acknowledgement: This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, Information and Communication Technologies (ICT) and Future Planning (NRF-2013R1A1A3008145).
 ===2005 [https://academic.oup.com/jid/article/191/12/2138/842542 The Cholinergic Anti-Inflammatory Pathway Regulates the Host Response during Septic Peritonitis]===