包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
5mg | 电议 |
100mg | 电议 |
Cell lines | Fresh bovine articular chondrocytes, sarcoplasmic reticulum |
Preparation method | The solubility of this compound in DMSO is >11.7 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Reacting condition | 1% or 2% lidocaine, 30 minutes |
Applications | Lidocaine (1%, 15-minute) decreased chondrocyte viability. Longer exposures to 1% and 2% lidocaine further reduced chondrocyte viability. Lidocaine (40 μM) showed reverse frequency-dependent depression of myocardial contractility. Lidocaine(40 μM, 100 μM) caused a marked depression of the late-peaking contractile responses, attributed to Ca2+ release from the sarcoplasmic reticulum. |
Animal models | Dogs with 2-hour-old myocardial infarctions |
Dosage form | Intravenous bolus injection, 2-8 μg/ml |
Application | Lidocaine prolonged the Q-EG intervals in the infarcted zones of the heart 17-26% at peak effect, but it had no effect on the Q-EG intervals in the normal zone except for a slight (1.5%) prolongation shortly after the initial intravenous bolus injection. Lidocaine prolonged the effective refractory period of the infarcted zone 23% at peak effect but had no effect on the effective refractory period of the normal zone. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
产品描述 | 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: |