Fig. 5

Lidocaine significantly inhibits morphine-induced inflammatory responses via a SOCS3-dependent way in BV-2 cells. a, b Real-time PCR showed suppressive effects of lidocaine on Il1b and Tnfa mRNA levels in morphine-stimulated BV-2 cells. Cells were pretreated with lidocaine (10 μM) for 12 h, followed by morphine (200 μM) treatment. Then, the cells were collected and analyzed 12 h after morphine treatment. c Effect of lidocaine on the phosphorylation of p38 MAPK in morphine-stimulated BV-2 cells. Cells were treated with lidocaine (10 μM) for 12 h before morphine (200 μM) treatment. d BV-2 cells were transfected with 100 pmol SOCS3 siRNA or control siRNA for 18 h, followed by 10 μM lidocaine treatment for 12 h. The efficiency of SOCS3 knockdown was assessed by immunoblot assay. e, f SOCS3 siRNA sufficiently abolished the anti-inflammatory effects of lidocaine on Il1b and Tnfa mRNA in BV-2 cells. BV-2 cells were transfected with 100 pmol SOCS3 siRNA or control siRNA and then subjected to 10 μM lidocaine pretreatment for 12 h, followed by exposure to morphine (200 μM) for 12 h. (a–f Data were obtained from three independent experiments). g Lidocaine (10 μM) inhibited the NF-κB translocation from the cytosol to the nucleus after morphine (200 μM) exposure for 1 h in BV-2 cells (n = 4). NF-κB activity was analyzed by p65 nuclear translocation assay. **p < 0.01 and ***p < 0.001 versus the vehicle group; ^# p < 0.05, ^## p < 0.01, and ^### p < 0.001 versus the morphine-treated group or lidocaine-treated group; ^&& p < 0.01 and ^&&& p < 0.001 versus the morphine and lidocaine-coadministered group. Scale bar 30 μm