Mauritio
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- Joined
- Feb 26, 2018
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Nicotine seems to have pro- and anti-inflammatory effects. Its increase in COX2 would be pro inflammatory.
On the other hand nicotine has some interesting anti-endotoxin effects, with endotoxin beeing one the biggest promoters of inflammation in the body.
This study suggests 2 mechanisms of nicotines anti endotoxin effect:
1. Nicotine stimulates α7 nAChR
("Nicotine stimulation of α7 nicotinic acetylcholine receptor (α7 nAChR) powerfully inhibits pro-inflammatory cytokine production in lipopolysaccharide (LPS)-stimulated macrophages and in experimental models of endotoxemia.")
2. Nicotine increases IRAK-M a kinase which lowers TLR related immune response a.k.a. inflammation.
Interestingly nicotine resulted in a state of "endotoxin intolerance" where endotoxin caused less of an inflammatory response.
Other studies:
Nicotine increases cox-2
Apigenin / orange juice to the rescue!
"Apigenin significantly inhibited the nicotine- and LPS-induced production of NO, PGE2, IL-1beta, TNF-alpha, IL-6, and IL-12, and the upregulation of iNOS and COX-2 in hPDL cells."
Nicotine is anti-endotoxin:
On the other hand nicotine has some interesting anti-endotoxin effects, with endotoxin beeing one the biggest promoters of inflammation in the body.
This study suggests 2 mechanisms of nicotines anti endotoxin effect:
1. Nicotine stimulates α7 nAChR
("Nicotine stimulation of α7 nicotinic acetylcholine receptor (α7 nAChR) powerfully inhibits pro-inflammatory cytokine production in lipopolysaccharide (LPS)-stimulated macrophages and in experimental models of endotoxemia.")
2. Nicotine increases IRAK-M a kinase which lowers TLR related immune response a.k.a. inflammation.
Interestingly nicotine resulted in a state of "endotoxin intolerance" where endotoxin caused less of an inflammatory response.
A New IRAK-M-Mediated Mechanism Implicated in the Anti-Inflammatory Effect of Nicotine via α7 Nicotinic Receptors in Human Macrophages
Nicotine stimulation of α7 nicotinic acetylcholine receptor (α7 nAChR) powerfully inhibits pro-inflammatory cytokine production in lipopolysaccharide (LPS)-stimulated macrophages and in experimental models of endotoxemia. A signaling pathway ...
www.ncbi.nlm.nih.gov
Other studies:
Nicotine increases cox-2
Change in nicotine-induced VEGF, PGE2 AND COX-2 expression following COX inhibition in human oral squamous cancer - PubMed
Cigarette smoke has been documented to be related to the development of cancer. However, the exact mechanism for the carcinogenic action of cigarette smoke is still unknown. Nicotine is recognized to be the major compound in cigarette smoke and has been suggested to play a role in oral cancer...
pubmed.ncbi.nlm.nih.gov
Nicotine augments glomerular injury in a rat model of acute nephritis - PubMed
Either in vivo or in vitro treatment with nicotine leads to activation of inflammatory mediators and hallmarks of glomerular injury, which may explain the mechanisms involved in the deleterious effects of cigarette smoking on renal disease.
pubmed.ncbi.nlm.nih.gov
Apigenin / orange juice to the rescue!
"Apigenin significantly inhibited the nicotine- and LPS-induced production of NO, PGE2, IL-1beta, TNF-alpha, IL-6, and IL-12, and the upregulation of iNOS and COX-2 in hPDL cells."
Anti-inflammatory effects of apigenin on nicotine- and lipopolysaccharide-stimulated human periodontal ligament cells via heme oxygenase-1 - PubMed
Apigenin possesses anti-inflammatory activity in hPDL cells and works through a novel mechanism involving the action of HO-1. Thus, apigenin may have potential benefits as a host modulatory agent in the prevention and treatment of periodontal disease associated with smoking and dental plaque.
pubmed.ncbi.nlm.nih.gov
Nicotine is anti-endotoxin:
Nicotine inhibits LPS-induced cytokine production and leukocyte infiltration in rat placenta - PubMed
These data show that nicotine suppresses LPS-induced placental inflammation by inhibition of cytokine release and infiltration of leukocytes into the placenta, and regulates the increased expression of α7-nAChR in placenta after LPS treatment. Nicotine and other nicotinic agonists may be an...
pubmed.ncbi.nlm.nih.gov
Nicotine protects fetus against LPS-induced fetal growth restriction through ameliorating placental inflammation and vascular development in late pregnancy in rats - PubMed
Our previous work has shown that nicotine suppressed lipopolysaccharide (LPS)-induced placental inflammation by inhibiting cytokine release as well as infiltration of leukocytes into the placenta through the cholinergic anti-inflammatory pathway. Nicotine also increased fetal survival and...
pubmed.ncbi.nlm.nih.gov
Nicotine, an α7 nAChR agonist, reduces lipopolysaccharide-induced inflammatory responses and protects fetuses in pregnant rats - PubMed
Nicotine reduces the LPS-induced inflammatory responses and rescues the fetus in rats during pregnancy. Thus, nicotine exerts dramatic antiinflammatory effects. These observations have important implications for control of inflammatory responses during pregnancy.
pubmed.ncbi.nlm.nih.gov