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with apoptosis by a network pharmacology approach. Subsequently, biological experiments validated that CTS inhibited ischemia/reperfusion-induced cardiomyocyte apoptosis in vivo and in vitro. Molecular docking techniques were used to screen key target information. Based on the simulative results, MAPKs were verified as well-connected molecules of CTS. Western blotting assays also demonstrated that CTS could enhance MAPK expression. Furthermore, we demonstrated that inhibition of the MAPK pathway reversed the CTS-mediated effect on card
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