ABSTRACT
The α4β2-nicotinic acetylcholine receptor (nAChR) is a ligand-gated ion channel that is distributed throughout the nervous system. It is involved in the regulation of various neurotransmitters including acetylcholine, dopamine, γ-aminobutyric acid, and norepinephrine. α4β2-nAChR plays an important role in learning, memory, cognition, attention, inflammation, and pain. A large number of studies have shown that α4β2-nAChR is an important therapeutic target for neurological diseases such as Alzheimer's disease, Parkinson's disease, epilepsy, depression, nicotine dependence, pain, etc. It is an important target in the early diagnosis and curative effect detection of neurodegenerative diseases including Alzheimer's disease. This review summarizes the role, mechanisms and related drug research advances on α4β2-nAChR ligand drugs in neurological diseases, as well as providing a theoretical basis for identifying and developing more suitable α4β2-nAChR-related compounds.
ABSTRACT
ObjectiveTo study the effect of α7 ( α7 AChR) agonist nicotine on regulating sensitivity of regular chemotherapeutic agent in cholangiocarcinoma cells,and explore the possible target.MethodsThe effect of nicotine and α-BTX pretreatment on the survival ability of cholangiocarcinoma cells was investigated when applied with 5-FU by using MTT and Flat cloning formation experiment.ResultsApplied with 5-FU,in various con centrations nicotine stimulating group( 10-3 g/L,10-4 g/L,10-5 g/L ),the survive rate of QBC939 was 128％,124％,118％,while that in α-BTX stimulating group and combined stimulation group was 92％,94％,93％,92％,respectively.The cloning formation ability of nicotine- stimulating group (6.2 ± 0.40) was significantly higher than α- BTX stimulating group (3.2 ± 0.20 ),combined stimulation group ( 3.2 ± 0.20 ) and control group ( 3.4 ±0.33).ConclusionNicotine can prevent chemotherapy-induced apoptosis,and improve cholangiocarcinoma cell survival via α7 nicotine acetylcholine receptor in vitro.