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Ginsenoside Rg1 can prevent adverse effects of lidocaine

Ginsenosides Rg1 activates neural stem cells
神經乾細胞 (neuralstemcell,NSCs)是一類具有分裂潛能和自更新能力的母細胞,它可以通過不對等的分裂方式產生神經組織的各類細胞。患病部位組織損傷後釋放各種趨化因子,可以吸引神經乾細胞聚集到損傷部位,並在局部微環境的作用下分化為不同種類的細胞,修復及補充損傷的神經細胞。因此,神經乾細胞具有廣泛的治療價值,可以用於各炎症或損傷導致的大腦神經細胞喪失(例如,老年癡呆、腦梗死後遺症、多發性硬化等)。 重慶醫科大學的研究發現:人參達瑪烷皂苷Rg1具有強烈的激發神經乾細胞的活性,並且進一步...
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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]

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