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1.
Journal of Biomedical Engineering ; (6): 224-231, 2021.
Article in Chinese | WPRIM | ID: wpr-879269

ABSTRACT

As a noninvasive neuromodulation technique, transcranial magnetic stimulation (TMS) is widely used in the clinical treatment of neurological and psychiatric diseases, but the mechanism of its action is still unclear. The purpose of this paper is to investigate the effects of different frequencies of magnetic stimulation (MS) on neuronal excitability and voltage-gated potassium channels in the


Subject(s)
Animals , Mice , Action Potentials , Magnetic Phenomena , Mental Disorders , Neurons , Patch-Clamp Techniques , Potassium Channels, Voltage-Gated
2.
Medical Journal of Chinese People's Liberation Army ; (12)2001.
Article in Chinese | WPRIM | ID: wpr-557009

ABSTRACT

Objective To study the expression of 9 delayed rectifier potassium channel subunits in human gastric cancer cell line AGS, as well as the effect of down-regulation of the expression of Kv1.5 on AGS cells proliferation. Methods RT-PCR technique was employed to detect the mRNA expression of Kv1.1, Kv1.2, Kv1.3, Kv1.5, Kv1.6, Kv2.1, Kv2.2, Kv3.1 and Kv3.2 in AGS cells. Once the expression of Kv1.5 protein was confirmed by immunofluorescence, small interference RNA (siRNA) was applied to down-regulate the Kv1.5 protein expression, then MTT assay and flow cytometry were used to observe the cell proliferation and the cell cycle distribution. Results Totally 7 delayed rectifier potassium channel subunits were detected in AGS cells, among them the mRNA levels of Kv1.3, Kv1.5 and Kv2.1 were much higher than that of the others. It was confirmed by immunofluorescence that the Kv1.5 protein was expressed mainly in AGS cytomembrane. After the endogenous Kv1.5 expression in AGS cells was down regulated by siRNA, the cell proliferation obviously slowed down and the cell growth stopped in G1 period. Conclusion Multiform expression of delayed rectifier potassium channel subunits existed in AGS cells, and Kv1.5 may be involved in the regulation of gastric carcinoma cell proliferation by modulating the cell cycle.

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