Lidocaine is a common local anesthetic and class-1b antiarrhythmic drug. Lidocaine is used topically to relieve itching, burning, and pain from skin inflammations, injected as a dental anesthetic, or as a local anesthetic for minor surgery.
Unfortunately, systemic intoxication and psychotic reaction associated with its use often occur because of its popularity and wider safety margin, for which guide in use is often ignored and overdose becomes commonplace. The CNS is the primary target organ for the toxic effects of lidocaine. Adverse effects of intravenous lidocaine include: headache, dizziness, drowsiness, confusion, visual disturbances, tinnitus, tremor, and/or paraesthesia. Neural cells exposed to lidocaine overdose will undertake apoptosis.
Chinese researchers found that ginsenoside Rg1 can markedly reduce apoptosis (programmed cell death) of neural cells exposed to lidocaine.
This study used modern technologies like TUNEL, flow cytometry to evaluate apoptosis of neural Jurkat cells. Results indicate Jurkat cells in the presence of Rg1 underwent less apoptosis. Further mechanism exploration discovered that the protective effect of Rg1 on lidocaine‑induced apoptosis is mediated by altering levels of BCL‑2 family proteins and downregulating caspase‑3 expression.
Protective effect of ginsenoside Rg1 on lidocaine-induced apoptosis.
Mol Med Rep. 2013 Nov 21;
Authors: Li H, Xu J, Wang X, Yuan G
Abstract
Lidocaine, as an anesthetic substance, is often used for surface and spinal anesthesia. However, studies have shown that lidocaine may induce transient neurological symptoms and cauda equina syndrome. In the present study the effects of the ginsenoside Rg1 (Rg1) on lidocaine‑induced apoptosis were assessed in Jurkat cells using flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The data showed that incubation with Rg1 provides protection against lidocaine‑induced apoptosis in cultured Jurkat cells. In order to investigate the effect of Rg1 on the apoptosis pathway, caspase 3 gene expression was determined. The results suggested that the protective effect of Rg1 on lidocaine‑induced apoptosis is mediated by altering the level of B‑cell lymphoma‑2 (BCL‑2) family proteins and downregulating caspase‑3 expression. In conclusion, the present study demonstrated that incubation with Rg1 provides protection against lidocaine‑induced apoptosis in cultured Jurkat cells. In addition, the study demonstrated that Rg1 is a notable antiapoptotic molecule that is capable of blocking the caspase‑dependent signaling cascade in Jurkat cells, and that the protective effect of Rg1 on lidocaine‑induced apoptosis is mediated by altering levels of BCL‑2 family proteins and downregulating caspase‑3 expression. The present study provides the basis for understanding and evaluating the effect of Rg1 in the in vivo treatment of lidocaine-induced transient neurological symptoms and cauda equina syndrome by lidocaine.
PMID: 24270314 [PubMed – as supplied by publisher]
