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Drug cardiotoxicity detection analysis method based on myocardial cell sensor

A technology of cardiomyocytes and cardiotoxicity, which is applied in the direction of analyzing materials, testing pharmaceutical preparations, and analyzing materials through optical means, which can solve the problems of inability to reflect the continuous and long-term change process of the heart, complex operation, and high cost. Long-term intuitive, simple operation steps, low cost effect

Inactive Publication Date: 2015-01-21
ZHEJIANG UNIV
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AI Technical Summary

Problems solved by technology

Isolated tissue and in vivo animal experiments can directly test the cardiotoxicity of drugs, but at the same time have the disadvantages of low throughput, complicated operation and high cost.
Biological methods of hERG inhibitors and receptor proteins cannot reflect the continuous and long-term changes in the heart after drug action

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  • Drug cardiotoxicity detection analysis method based on myocardial cell sensor
  • Drug cardiotoxicity detection analysis method based on myocardial cell sensor
  • Drug cardiotoxicity detection analysis method based on myocardial cell sensor

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Embodiment Construction

[0031] The present invention will be described in further detail below in conjunction with the accompanying drawings and specific embodiments, but the present invention is not limited.

[0032] The drug cardiotoxicity detection and analysis method based on the cardiomyocyte sensor of the present invention, the method is realized on the drug cardiotoxicity detection and analysis system, such as figure 1 As shown, the drug cardiotoxicity detection and analysis system includes: a cardiomyocyte sensor culture plate 1, an upright microscope 3, a CCD camera 4 and a computer 5; wherein, cardiomyocytes are attached to the surface of the cardiomyocyte sensor culture plate 1; The sensor culture plate 1 is fixed on the stage of the upright microscope 3; the CCD camera 4 is fixed on the top of the upright microscope 3; the CCD camera 4 is connected with the computer 5 through the USB connection line 2, so that the acquisition signal is transmitted to the computer 5 for further processing. ...

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Abstract

The invention discloses a drug cardiotoxicity detection analysis method based on a myocardial cell sensor. According to the drug cardiotoxicity detection analysis method, a high-performance and low-cost cardiac muscle cell sensor is constructed by adopting ex vivo myocardial cell culture; the change of pulsation images when myocardial cells mechanically pulsate is calculated and detected by adopting algorithms such as image acquisition, conversion of an RGB image into a gray level image, image binaryzation, image matrixing and peak detection, and the mechanical pulsation of the myocardial cells is quantized by using a difference value of the pulsation images, the detection on a rate, an amplitude and a pulsation interval of mechanical pulsation of the myocardial cells is realized; by analyzing the change of the mechanical pulsation state of the myocardial cells over time under the drug action, the cardiotoxicity of a drug is evaluated. Compared with an existing drug cardiotoxicity detection analysis method, the drug cardiotoxicity detection analysis method has the advantages of no marks, no loss, low cost, simple operating steps, and the like, and is capable of observing and evaluating the drug cardiotoxicity simply for a long time.

Description

technical field [0001] The invention relates to a drug cardiotoxicity detection and analysis technology, in particular to a drug cardiotoxicity detection and analysis method based on a cardiomyocyte sensor. Background technique [0002] Cardiac safety is the most concerned issue in the development, approval and use of new drugs, but many drugs are currently restricted or withdrawn from the market due to heart safety problems, resulting in drug loss. Torsades de pointes (TdP) is a side effect of most drugs on the heart. TdP is a ventricular tachycardia with an oscillating pattern near baseline on the ECG. TdP is caused by a fast delayed rectifier K on the cardiomyocyte membrane + The ion channel IKr is inhibited, and IKr is encoded by the human ether-a-go-go-related gene (hERG). IKr is the major repolarizing current in human ventricular myocytes, and when inhibited, causes prolonged depolarization and repolarization, ultimately leading to TdP. Therefore, drug candidates i...

Claims

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Application Information

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IPC IPC(8): G01N21/84G01N33/15
Inventor 王平苏凯麒胡宁王琴邹玲黎洪波邹瞿超曹端喜
Owner ZHEJIANG UNIV
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