The protective effect of lipid emulsion in preventing bupivacaine-induced mitochondrial injury and apoptosis of H9C2 cardiomyocytes

Abstract Anshen Buxin Liuwei pill (ABLP), a Mongolian medicinal formula, composed of the six medicinal materials of Mongolian medicine Bos taurus domesticus Gmelin, Choerospondias axillaris (Roxb. ) Burtt et Hill, Myristica fragrans Houtt., Eugenia caryophµllata Thunb., Aucklandia lappa Decne., Liqui dambar formosana Hance, is considered to have a therapeutic effect on the symptoms such as coronary heart disease, angina pectoris, arrhythmia, depression and irritability, palpitation, and shortness of breath. Therefore, the present study was employed a network pharmacology approach to identify the potentially active ingredients and to evaluate the protective effect of ABLP on hypoxia/reoxygenation (HR)-induced H9c2 cardiomyocytes, and its influence on cell viability, apoptosis, oxidative stress. H9c2 cardiomyocytes were used to construct a HR injury model. CCK-8 assay and AnnexinV-FITC cell apoptosis assays were used for cell viability and cell apoptosis determination. The levels of LDH, SOD, MDA, CAT, CK, GSH-Px, Na+-K+-ATPase, and Ca2+-ATPase in the cells were determined to assess the effect of ABLP. the mRNA levels of Sirtuin3 (Sirt3) and Cytochrome C (Cytc) in H9c2 cells were determined by quantitative real-time PCR. The finding of this study indicates that HR treatment cells began to shrink from the spindle in an irregular shape with some floated in the medium, well by increasing the therapeutic dose of ABLP (5 µg/mL, 25 µg/mL, and 50 µg/mL), the cells gradually reconverted in a concentration-dependent manner. The release of CK in HR-treated cells was significantly increased, indicating that ABLP exerts a protective effect in H9c2 cells against HR injury and can improve the mitochondrial energy metabolism and mitochondrial function integrity. The present study scrutinized the cardio-protective effect of ABLP against the HR-induced H9c2 cells injury through antioxidant and mitochondrion pathways. ABLP could be a promising therapeutic drug for the treatment of myocardial ischemic cardiovascular disease. The results will provide reasonable information for clinical use of the ABLP.

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Cox-2 Negatively Affects the Protective Role of Propofol against Hypoxia/Reoxygenation Induced Cardiomyocytes Apoptosis through Suppressing Akt Signaling

BioMed Research International ◽

10.1155/2019/7587451 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9

Author(s):

Kangmu Ma ◽

Jiapei Qiu ◽

Mi Zhou ◽

Yang Yang ◽

Xiaofeng Ye

Keyword(s):

Protective Effect ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Protective Role ◽

Akt Phosphorylation ◽

Over Expression ◽

H9c2 Cardiomyocytes ◽

Cox 2 ◽

Myocardial Ischemia Reperfusion ◽

Hypoxia Reoxygenation

Nowadays, the prevention of severe myocardium injury resulting from myocardial ischemia/reperfusion injury (I/R) has been recognized as an important subject in the field of ischemic heart disease. In this study, H9c2 cardiomyocytes were exposed to cycles of hypoxia/reoxygenation (H/R) to mimic myocardial I/R injury. Western blot analysis and qRT-PCR were performed to detect the expression of Cox-2, Akt and p-Akt. Cell viability, LDH release and activity of Caspase-3 were assessed to determine the protective effect of propofol. The results proved that the protective effect of propofol for H/R challenged cardiomyocytes was associated with Akt phosphorylation. We also revealed that treatment of propofol suppressed the expression of Cox-2 in cardiomyocytes which was up-regulated after H/R treatment. Conversely, the over-expression of Cox-2 inhibited Akt phosphorylation while enhancing cardiomyocytes apoptosis. Interestingly, Akt activator exhibited similar protective effect with propofol and could diminish the influences brought by over-expression of Cox-2. Thus, it could be concluded that Cox-2 negatively affects the protective effect of propofol against hypoxia/reoxygenation induced cardiomyocyte apoptosis by suppressing Akt phosphorylation.

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Protective effect of Tianqi Hangli Recipe (天芪航力方) extract on high sustained positive acceleration stress-induced myocardial mitochondrial injury in rats

Chinese Journal of Integrative Medicine ◽

10.1007/s11655-014-1835-1 ◽

2014 ◽

Cited By ~ 1

Author(s):

Liang-en Chen ◽

Feng Wu ◽

Yi-mei Xin ◽

An-dong Zhao ◽

Yong-xin Wang ◽

...

Keyword(s):

Protective Effect ◽

Mitochondrial Injury ◽

Positive Acceleration ◽

Acceleration Stress

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Protective Effect of Pyrroloquinoline Quinone on TNF-α-induced Mitochondrial Injury in Chondrocytes

Current Medical Science ◽

10.1007/s11596-020-2248-3 ◽

2021 ◽

Vol 41 (1) ◽

pp. 100-107

Author(s):

Guang-tao Han ◽

Wei-song Cai ◽

Yu-biao Zhang ◽

Si-qi Zhou ◽

Bin He ◽

...

Keyword(s):

Protective Effect ◽

Pyrroloquinoline Quinone ◽

Mitochondrial Injury ◽

Tnf Α

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Sevoflurane Postconditioning Attenuates Hypoxia/Reoxygenation Injury of Cardiomyocytes Under High Glucose by Regulating HIF-1α/MIF/AMPK Pathway

Frontiers in Pharmacology ◽

10.3389/fphar.2020.624809 ◽

2021 ◽

Vol 11 ◽

Author(s):

Haiping Ma ◽

Yongjie Li ◽

Tianliang Hou ◽

Jing Li ◽

Long Yang ◽

...

Keyword(s):

Membrane Potential ◽

Protective Effect ◽

Cell Viability ◽

Mrna Expression ◽

High Glucose ◽

Mitochondrial Membrane ◽

Ampk Signaling ◽

H9c2 Cardiomyocytes ◽

Reoxygenation Injury ◽

Hypoxia Reoxygenation

Subject: Cardiovascular disease, as a very common and serious coexisting disease in diabetic patients, and is one of the risk factors that seriously affect the prognosis and complications of surgical patients. Previous studies have shown that sevoflurane post-conditioning (SPostC) exerts a protective effect against myocardial ischemia/reperfusion injury by HIF-1α, but the protective effect is weakened or even disappeared under hyperglycemia. This study aims to explore whether regulating the HIF-1α/MIF/AMPK signaling pathway can restore the protective effect and reveal the mechanism of SPostC on cardiomyocyte hypoxia/reoxygenation injury under high glucose conditions.Methods: H9c2 cardiomyocytes were cultured in normal and high-concentration glucose medium to establish a hypoxia/reoxygenation (H/R) injury model of cardiomyocytes. SPostC was performed with 2.4% sevoflurane for 15 min before reoxygenation. Cell damage was determined by measuring cell viability, lactate dehydrogenase activity, and apoptosis; Testing cell energy metabolism by detecting reactive oxygen species (ROS) generation, ATP content and mitochondrial membrane potential; Analysis of the change of HIF-1α, MIF and AMPKα mRNA expression by RT-PCR. Western blotting was used to examine the expression of HIF-1α, MIF, AMPKα and p-AMPKα proteins. HIF-1α and MIF inhibitors and agonists were administered 40 min before hypoxia.Results: 1) SPostC exerts a protective effect by increasing cell viability, reducing LDH levels and cell apoptosis under low glucose (5 μM) after undergoing H/R injury; 2) High glucose concentration (35 μM) eliminated the cardioprotective effect of SPostC, which is manifested by a significantly decrease in the protein and mRNA expression level of the HIF-1α/MIF/AMPK signaling pathway, accompanied by decreased cell viability, increased LDH levels and apoptosis, increased ROS production, decreased ATP synthesis, and decreased mitochondrial membrane potential; 3. Under high glucose (35 μM), the expression levels of HIF-1α and MIF were up-regulated by using agonists, which can significantly increase the level of p-AMPKα protein, and the cardioprotective effect of SPostC was restored.Conclusion: The signal pathway of HIF-1α/MIF/AMPK of H9c2 cardiomyocytes may be the key point of SPostC against H/R injure. The cardioprotective of SPostC could be restored by upregulating the protein expression of HIF-1α and MIF under hyperglycemia.

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Protective effect ofMutellina purpureapolyphenolic compounds in doxorubicin-induced toxicity in H9c2 cardiomyocytes

Drug and Chemical Toxicology ◽

10.3109/01480545.2014.893443 ◽

2014 ◽

Vol 38 (1) ◽

pp. 1-8 ◽

Cited By ~ 4

Author(s):

Slawomir Mandziuk ◽

Tomasz Baj ◽

Elwira Sieniawska ◽

Jaroslaw Dudka ◽

Renata Gieroba ◽

...

Keyword(s):

Protective Effect ◽

H9c2 Cardiomyocytes

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Abstract 221: Autophagy is Involved in the Protective Effect of Endophilin A2 on H 2 O 2 -induced Apoptosis in H9C2 Cardiomyocytes

Circulation Research ◽

10.1161/res.123.suppl_1.221 ◽

2018 ◽

Vol 123 (Suppl_1) ◽

Author(s):

Yun Liu ◽

Hai-Qi Liu ◽

Xin-Qiu-Yue Wang ◽

Huan-Jia Shen

Keyword(s):

Protective Effect ◽

H9c2 Cardiomyocytes ◽

Induced Apoptosis

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Protective effect of inhibiting TRPM7 expression on hypoxia post-treatment H9C2 cardiomyocytes

Clinical Hemorheology and Microcirculation ◽

10.3233/ch-200934 ◽

2020 ◽

pp. 1-15

Author(s):

Juesheng Yang ◽

Shan Hu ◽

Li Huang ◽

Jianliang Zhou ◽

Haiyan Xiang ◽

...

Keyword(s):

Protective Effect ◽

Reperfusion Injury ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Transient Receptor Potential Channel ◽

Post Treatment ◽

Ion Concentration ◽

H9c2 Cells ◽

H9c2 Cardiomyocytes ◽

Transient Receptor

BACKGROUND: Transient receptor potential channel 7 (TRPM7) plays an important role in maintaining intracellular ion concentration and osmotic pressure. OBJECTIVE: The purpose of this study was to investigate the role and mechanism of inhibiting the expression of TRPM7 in the treatment of distal myocardial ischemia. METHODS: H9C2 cells were treated with hypoxia post-treatment and reperfusion, respectively, detect the expression of HIF-1α and TRPM7, the concentration of Ca2 + and the degree of apoptosis in the H9C2 cells. The relevant miRNAs targeting TRPM7 were searched, the TRPM7 interference vectors were constructed, and the interference of different interference vectors on TRPM7 in H9C2 cells was detected. RESULTS: The results showed that hypoxia post-treatment treatment would lead to increased expression of miR-22-3p which directly targeting TRPM7, decreased expression of TRPM7, increased expression of HIF-α and increased intracellular Ca2 + concentration. While reperfusion can increase the expression of HIF-1α and TRPM7 in H9C2 cells and increase the degree of apoptosis. CONCLUSION: Knockdown of TRPM7 can significantly reduce reperfusion injury in H9C2 cells, reduce the degree of apoptosis, and the TRPM7 interference vector can inhibit the expression of TRPM7 and have a certain protective effect on the reperfusion injury of H9C2 cells.

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