Qishen Yiqi Drop Pill, a novel compound Chinese traditional medicine protects against high glucose‐induced injury in cardiomyocytes

Autor: Lijun Zhang, Lixia Li, Xiaochun Qing, Ming-Ming Zhang, Hao Wang, Zhuo Zhang, Shouyan Zhang, Xue-Wei Chang, Hui-Fang Ma
Rok vydání: 2019
Předmět:
0301 basic medicine
high glucose injury
Cell Survival
Apoptosis
Pharmacology
Protective Agents
Mitochondrial Membrane Transport Proteins
Cell Line
traditional Chinese medicine
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Western blot
Qishen Yiqi Drop Pill
medicine
Animals
Myocytes
Cardiac
LY294002
Viability assay
Medicine
Chinese Traditional
Protein kinase B
PI3K/AKT/mTOR pathway
Membrane Potential
Mitochondrial
chemistry.chemical_classification
PI3K/Akt
Reactive oxygen species
medicine.diagnostic_test
Mitochondrial Permeability Transition Pore
Original Articles
Cell Biology
Rats
Glucose
030104 developmental biology
chemistry
Mitochondrial permeability transition pore
diabetes cardiomyopathy
030220 oncology & carcinogenesis
Molecular Medicine
Original Article
Reactive Oxygen Species
Drugs
Chinese Herbal
Signal Transduction
Zdroj: Journal of Cellular and Molecular Medicine
ISSN: 1582-4934
1582-1838
DOI: 10.1111/jcmm.14527
Popis: Objective Qishen Yiqi Drop Pill (QSYQ) has been recognized as a potential protective agent for various cardiovascular diseases. However, the effect of QSYQ in cardiac complications associated with diabetes is not clear currently. In this study, we investigate whether QSYQ could exert cardiac protective effects against high glucose‐induced injuries in cardiac H9c2 cells. Methods H9c2 cells were exposed to 24 hours of high glucose in presence or absence of QSYQ and LY294002. Cell cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, mitochondrial membrane potential and mitochondrial permeability transition pore (mPTP) opening were determined. Levels of bax, bcl‐2, p53, cleaved caspase‐3, PI3K and Akt were evaluated by Western blot. Results Our data indicated that QSYQ significantly increased the cell viability and decreased cytotoxicity. By analysing the apoptotic rate as well as the expression levels of cytoapoptosis‐related factors including cleaved caspase‐3, bax, bcl‐2, and p53, we found that QSYQ could remarkably suppress apoptosis of cardiomyoblasts caused by high glucose. In addition, it also showed that QSYQ reduced the generation of ROS. We further found that QSYQ treatment could inhibit the loss of mitochondrial membrane potential and mPTP opening. Moreover, Western blot analysis showed enhanced phosphorylation of PI3K/Akt. The specific inhibitor of PI3K, LY294002 not only inhibited QSYQ induced PI3K/Akt signalling pathway activation, but alleviated its protective effects. Conclusions In summary, these findings demonstrated that QSYQ effectively protected H9c2 cells against the series injuries due to high glucose at least partially by activating the PI3K/Akt signalling pathway.
Databáze: OpenAIRE
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