Lidocaine (Lignocaine) inhibits sodium channels involving complex voltage and using dependence[1]. Lidocaine decreases growth, migration and invasion of gastric carcinoma cells via up-regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways. Lidocaine is a commonly used local anesthetics of amide derivative, a drug to treat ventricular arrhythmia and an effective tumor-inhibitor[2].
Lidocaine (Lignocaine) (10 nM; 48 hours) decreases significantly cell proliferation[2]. Lidocaine (1-10 nM; 24-72 hours) inhibits cell viability and achieves the most suppressing effects at the concentration of 10 nM and treatment time 48 hours[2]. Lidocaine (10 nM; 48 hours) increases significantly the apoptotic cell rate[2]. Lidocaine (10 nM; 48 hours) down-regulates Cyclin D1 and up-regulates p21 expression significantly[2].
Lidocaine (Lignocaine) causes completely reversible tail nerve block in rats. Mechanical nociception block produced by lidocaine has slower onset and faster recovery compared with thermal nociception block[3].
References:
[1]. Cummins TR, et al. Setting up for the block: the mechanism underlying lidocaine's use-dependent inhibition of sodium channels. J Physiol. 2007 Jul 1;582(Pt 1):11.
[2]. Sui H, et al. Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145. BMC Cancer. 2019 Mar 15;19(1):233.
[3]. Li Z, et al. Evaluation of the antinociceptive effects of lidocaine and bupivacaine on the tail nerves of healthy rats. Basic Clin Pharmacol Toxicol. 2013 Jul;113(1):31-6.