AKT1 and myocarditis: α-CTX AuIB and LY294002, on the contrary, reversed the therapeutic function of nicotine, and the inflammatory infiltrates in these two groups were even worse than those in the CVB3-infected group, indicating that nicotine has an anti-inflammatory action in the murine model of CVB3-induced myocarditis through the α3β4-nAChR/PI3K/Akt-dependent pathway.