• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

Activation of Ca2+/Calmodulin-Dependent Protein Kinase II (CaMKII) with Lidocaine Provokes Pyroptosis of Glioblastoma Cells
The study examines the problem whether pyroptosis of U87-MG glioblastoma cells can result from activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) by a local anesthetic. Glioblastoma cells exposed to various concentrations of typical local anesthetic lidocaine demonstrated augmented cytosolic flux of Ca2+, while suppression of CaMKII expression with the corresponding siRNA significantly inhibited this effect in cells treated with 2 mM lidocaine. Lidocaine up-regulated the expression of mRNA caspase-3 and gasdermin GSDME proteins, whereas silencing of CaMKII gene with siRNA significantly moderated this effect...
Source: Bulletin of Experimental Biology and Medicine - July 24, 2021 Category: Biology Source Type: research

Lidocaine inhibits the metastatic potential of ovarian cancer by blocking NaV1.5 ‐mediated EMT and FAK/Paxillin signaling pathway
This study aims to investigate whether lidocaine inhibits the malignancy of ovarian cancer through NaV1.5 blockage. Human ovarian cancer, its metastatic cancer and normal ovarian tissues were probed with anti ‐NaV1.5 antibodyin situ. Human ovarian cancer A2780 and SKOV3 cells were cultured and their growth, epithelial ‐mesenchymal transition (EMT), migration, and invasion in the presence or absence of lidocaine together with underlying molecular mechanisms were assessed. Murine syngeneic ovarian cancer (ID8) model was also used to determine the chemotherapeutic efficiency of cisplatin in combination with lidoca ine. Th...
Source: Cancer Medicine - December 6, 2020 Category: Cancer & Oncology Authors: Chang Liu, Ming Yu, Yi Li, Hao Wang, Chuanya Xu, Xiaoqing Zhang, Min Li, Hongyan Guo, Daqing Ma, Xiangyang Guo Tags: ORIGINAL RESEARCH Source Type: research

H1R mediates local anesthetic-induced vascular permeability in angioedema.
This study supported a key role of H1R in LA-induced angioedema, and suggested that in the design of LA structure, the ring formation of the N-methyl scaffold on the side chain can properly avoid the angioedema. PMID: 32061592 [PubMed - as supplied by publisher]
Source: Toxicology and Applied Pharmacology - February 11, 2020 Category: Toxicology Authors: Cao J, Zhang Y, Che D, Liu R, Yang L, Zhang T, He L Tags: Toxicol Appl Pharmacol Source Type: research

Autophagy activated by tuberin/mTOR/p70S6K suppression is a protective mechanism against local anaesthetics neurotoxicity.
Abstract The local anaesthetics (LAs) are widely used for peripheral nerve blocks, epidural anaesthesia, spinal anaesthesia and pain management. However, exposure to LAs for long duration or at high dosage can provoke potential neuronal damages. Autophagy is an intracellular bulk degradation process for proteins and organelles. However, both the effects of LAs on autophagy in neuronal cells and the effects of autophagy on LAs neurotoxicity are not clear. To answer these questions, both lipid LAs (procaine and tetracaine) and amide LAs (bupivacaine, lidocaine and ropivacaine) were administrated to human neuroblasto...
Source: J Cell Mol Med - November 14, 2016 Category: Molecular Biology Authors: Xiong J, Kong Q, Dai L, Ma H, Cao X, Liu L, Ding Z Tags: J Cell Mol Med Source Type: research

Autophagy activated by tuberin/mTOR/p70S6K suppression is a protective mechanism against local anaesthetics neurotoxicity
Abstract The local anaesthetics (LAs) are widely used for peripheral nerve blocks, epidural anaesthesia, spinal anaesthesia and pain management. However, exposure to LAs for long duration or at high dosage can provoke potential neuronal damages. Autophagy is an intracellular bulk degradation process for proteins and organelles. However, both the effects of LAs on autophagy in neuronal cells and the effects of autophagy on LAs neurotoxicity are not clear. To answer these questions, both lipid LAs (procaine and tetracaine) and amide LAs (bupivacaine, lidocaine and ropivacaine) were administrated to human neuroblastoma SH‐S...
Source: Journal of Cellular and Molecular Medicine - October 31, 2016 Category: Molecular Biology Authors: Jingwei Xiong, Qiuyue Kong, Leyang Dai, He Ma, Xiaofei Cao, Li Liu, Zhengnian Ding Tags: Original Article Source Type: research

Inhibition of long non-coding RNA IGF2AS has profound effect on inducing neuronal growth and protecting local-anesthetic induced neurotoxicity in dorsal root ganglion neurons
Conclusions Inhibiting endogenous IGF2AS may promote neuronal growth and protect local-anesthetic induced neurotoxicity in DRG neurons, possibly through complimentary IGF2 upregulation and autocrine activation neurotrophin genes.
Source: Biomedicine and Pharmacotherapy - May 17, 2016 Category: Drugs & Pharmacology Source Type: research

Amitriptyline Activates TrkA to Aid Neuronal Growth and Attenuate Anesthesia-Induced Neurodegeneration in Rat Dorsal Root Ganglion Neurons
Abstract: Tricyclic antidepressant amitriptyline (AM) has been shown to exert neurotrophic activity on neurons. We thus explored whether AM may aid the neuronal development and protect anesthesia-induced neuro-injury in young spinal cord dorsal root ganglion (DRG) neurons. The DRG explants were prepared from 1-day-old rats. The effect of AM on aiding DRG neural development was examined by immunohistochemistry at dose-dependent manner. AM-induced changes in gene and protein expressions, and also phosphorylation states of tyrosine kinases receptor A (TrkA) and B (TrkB) in DRG, were examined by quantitative real-time polymer...
Source: Medicine - May 1, 2016 Category: Internal Medicine Tags: Research Article: Meta-Analysisof Observ Studiesin Epidemiology Source Type: research

GNB2 is a mediator of lidocaine-induced apoptosis in rat pheochromocytoma PC12 cells.
Abstract Lidocaine has been recognized to induce neurotoxicity. However, the molecular mechanism underlying this effect, especially the critical molecules in cells that mediated the lidocaine-induced apoptosis were unclear. In the present study, PC12 cells were administrated with lidocaine for 48h. Using MTT assay and flow cytometry, we found lidocaine significantly decreased the cell proliferation and S phases in PC12 cells with treatment concentrations, and significantly enhanced cell apoptosis with treatment concentrations. Two-dimensional gel electrophoresis (2-DE) analysis and LC-MS/MS were used to identifica...
Source: Neurotoxicology - March 22, 2016 Category: Neurology Authors: Tan Y, Wang Q, Zhao B, She Y, Bi X Tags: Neurotoxicology Source Type: research