Medicine Cardiac Toxicity Assessment Service
With the development of biotechnology, more and more drugs will enter the market. However, some drugs have the potential for myocardial cell toxicity, which may seriously cause the risk of cardiovascular diseases such as heart failure, myocardial hypertrophy, and congestive heart failure.
Creative Bioarray provides our clients with drugs myocardial cytotoxicity assessment services. We provide drug administration experiments, pharmacology, efficacy evaluation, and pharmacokinetic analysis, and evaluate whether the candidate drugs provided by customers can cause oxidative stress/damage at the cellular level and organelle level (mainly endoplasmic reticulum and mitochondria), and quantify the toxicity of the drugs to myocardial cells.
Service Case
Drug X is a drug that will be used to treat type 2 diabetes and insulin resistance in the clinic. However, experiments have shown that drug X has the risk of cardiovascular diseases such as heart failure, myocardial hypertrophy, and congestive heart failure. Its specific cardiotoxic characteristics and mechanisms need to be clarified, which is suspected to be related to mitochondrial oxidative stress.
Experimental scheme
We used human cardiomyocytes cultured in Vitro to reveal the characteristics of drug x-induced myocardial cytotoxicity, and evaluated its potential toxic mechanism from the perspective of mitochondrial oxidative stress and autophagy.
Service Content
We cultured the myocardial cell lines provided by our customers, digested the cells in the logarithmic growth stage with trypsin, and resuspended them. After inoculation and culture, different concentrations of drug X were added.
- After treatment a while, the cells treated with the drug were placed under an inverted microscope to observe the morphological changes of each group of cells and collect pictures.
- The cell survival rate was detected by the CCK-8 method, the absorbance was detected by a microplate reader and the cell survival rate was calculated.
- LDH release was detected by the leakage method to determine whether the drug would damage the membrane integrity.
- High content living cell imaging was used to detect mitochondrial membrane potential to determine whether drug X could induce mitochondrial dysfunction in myocardial cells in a concentration-dependent manner.
- The content of ROS was detected by high content living cell imaging to determine the level of cell stress.
- The levels of autophagy-related proteins were detected by Western blot.
Empirical Conclusion
The research suggests that the toxic mechanism of drug X may be related to its induction of ROS production. Excessive ROS can not only change gene and protein expression, affect cell function and phenotype but also attack important components such as nucleic acid, protein, and lipid in cells, inhibit mitochondrial biosynthesis, and further aggravate mitochondrial dysfunction, and eventually cause cell apoptosis. The results of this study showed that the mitochondrial membrane potential decreased and the whole-cell ROS content increased after administration of drug X, suggesting that the toxic effect of drug X on myocardial cells may promote oxidative stress injury by activating the mitochondrial pathway.
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