Oxygen inhalation was given to mice at 4?and 12 h after zymosan injection. One group of mice?underwent vagotomy 7 d before zymosan injection. The other two groups of mice either received nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine, or ¦Á7 nicotinic acetylcholine receptor (¦Á7nAChR) antagonist methyllycaconitine 30 min before oxygen was given.
The 100 % oxygen treatment significantly decreased the serum level of TNF-¦Á and increased the serum level of IL-10. The pathologic changes of the heart, lung, liver, and kidney were attenuated, as well as the dysfunction of liver and kidney. The 7-d survival rate of zymosan-challenged mice was also improved. Conversely, all these protective effects caused by pure oxygen treatment were abolished in?those animals that received anti-cholinergic treatments.
The cholinergic anti-inflammatory pathway may be involved in the 100 % oxygen protective mechanism against zymosan-induced generalized inflammation in mice.