SYKT Alleviates Doxorubicin-Induced Cardiotoxicity via Modulating ROS-Mediated p53 and MAPK Signal Pathways

Evidence-based Complementary and Alternative Medicine : ECAM
Ting ChenWenhui Li

Abstract

Backgrounds. Doxorubicin (DOX) is an effective therapeutic drug for malignant tumors; however, its clinical applications were limited by its side effects, especially the cardiotoxicity caused by ROS-mediated p53 and MAPK signal pathways' activation-induced cell apoptosis. Sanyang Xuedai mixture (SYKT) has been reported as an antioxidant agent and attenuated DOX-induced cardiotoxicity by targeting ROS-mediated apoptosis, but the mechanisms are still not fully delineated. Objective. This study aimed at investigating whether SYKT alleviated DOX-induced cardiotoxicity by inhibiting ROS-mediated apoptosis and elucidating the role of ROS-mediated p53 and MAPK signal pathways' activation in this process. Materials and Methods. Identification, separation, and culture of mouse primary cardiomyocytes. Cells were treated with DOX (1 μM), SYKT (30 mg/mL), or SYKT coupled with DOX. The p53 inhibitor Pifithrin-α (PFT-α), p38/MAPK inhibitor SB203583 (SB), and JNK inhibitor SP600125 (SP) were used as positive control. Western blot was employed to detected p53 and p38 as well as JNK expressions and the activation and translocation of Bax and cytochrome C. Flow cytometer (FCM) was used to detect the mitochondrial membrane potential and cell apop...Continue Reading

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Citations

Oct 16, 2019·Frontiers in Pharmacology·Danqi ChangYanggan Wang
Nov 22, 2018·Frontiers in Pharmacology·Qing-Yu ZhangLing-Dong Kong
Jun 5, 2021·Nutrition and Cancer·Mahboobeh Ghasemzadeh RahbardarHossein Hosseinzadeh

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Methods Mentioned

BETA
dissection
flow cytometry

Software Mentioned

SPSS
Image
Pro Plus

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