Effects of endomorphin-1 postconditioning on myocardial ischemia/reperfusion injury and myocardial cell apoptosis in a rat model

Zhang, Weiping; Zong, Qiao‐Feng; Gao, Qin; Yu, Ying; Gu, Xiaolei; Ya, Wang; Li, Zhenghong; Ge, Min

doi:10.3892/mmr.2016.5695

Cited by 23 publications

(25 citation statements)

References 30 publications

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“…NO, the main effect of the expansion of blood vessels, attenuates myocardial ischemia (22). SOD can resist cell damage caused by oxygen free radicals and timely repair of damaged cells, reflecting the body's ability to clear free radicals, in particular, to reflect the capacity of clearing superoxide anion (23). Increased levels of NO and SOD partly contribute towards the action of DIM to attenuate cardiomyocyte hypoxia injury.…”

Section: Discussionmentioning

confidence: 99%

3,3′-Diindolylmethane attenuates cardiomyocyte hypoxia by modulating autophagy in H9c2 cells

Liang

Qian

Zong

2017

Molecular Medicine Reports

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Autophagy is activated in the ischemic heart and is a process that is essential for survival, differentiation, development and homeostasis. 3,3'‑Diindolylmethane (DIM) is a natural product of the acid‑catalyzed condensation of indole‑3‑carbinol in cruciferous vegetables. Numerous studies have suggested that DIM has various pharmacological effects, including antioxidant, antitumor, anti‑angiogenic and anti‑apoptotic properties. However, the function of DIM on hypoxia‑induced cardiac injury remains to be elucidated. In the present study, H9c2 cells were pretreated with DIM (1, 5 and 10 µM) for 12 h and exposed to hypoxia for 12 h. It was demonstrated that DIM markedly attenuated the increased transcription of interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α induced by hypoxia. In addition, the transcription of autophagy associated genes increased in the DIM pretreated group, compared with the hypoxia group. DIM additionally attenuated the increased apoptosis, as determined by terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and regulated the relative protein expression level of B cell lymphoma (Bcl) 2 associated X protein, Bcl‑xL and cleaved caspase 3. Furthermore, the phosphorylation of the 5' AMP‑activated protein kinase a (AMPKa) was activated and the phosphorylation of c‑Jun N‑terminal kinase (JNK) was inhibited. The effect of DIM on hypoxia‑induced apoptosis was abolished following pretreatment with JNK activator (anisomycin, 40 ng/ml). The effect of DIM on autophagy was reversed following pretreatment with AMPKa inhibitor (CpC, 20 µM) following stimulation with hypoxia. The results demonstrated that DIM prevented hypoxia‑induced inflammation and apoptosis and activated cardiomyocyte autophagy, which may be mediated by activation of AMPKa and inhibition of JNK pathways.

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Section: Discussionmentioning

confidence: 99%

3,3′-Diindolylmethane attenuates cardiomyocyte hypoxia by modulating autophagy in H9c2 cells

Liang

Qian

Zong

2017

Molecular Medicine Reports

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“…For the control group, 2 mL of DMEM/F-12 medium containing 10% FBS was added to the 6-well plate. [25][26][27][28][29][30][31][32][33][34][35] and 10% FBS containing NSC-CPM were added to the 6-well plate, with the final concentration of Aβ 25-35 40 µM. The isolation and culturing of the NSCs and the NSC-CDM were performed according to our previous study [12].…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Neural stem cell-conditioned medium ameliorates Aβ25–35-induced damage in SH-SY5Y cells by protecting mitochondrial function

Jia

Diao

Liu

et al. 2020

Bosn J of Basic Med Sci

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Inhibition of amyloid β (Aβ)-induced mitochondrial damage is considered crucial for reducing the pathological damage in Alzheimer’s disease (AD). We evaluated the effect of neural stem cell-conditioned medium (NSC-CDM) on Aβ25–35-induced damage in SH-SY5Y cells. An in vitro model of AD was established by treating SH-SY5Y cells with 40 μM Aβ25–35 for 24 h. SH-SY5Y cells were divided into control, Aβ25–35 (40 μM), Aβ25–35 (40 μM) + NSC-CDM, and Aβ25–35 (40 μM) + neural stem cell-complete medium (NSC-CPM) groups. Cell viability was detected by CCK-8 assay. Apoptosis, reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP) were detected by flow cytometry. Malondialdehyde (MDA) content was detected by ELISA assay. Western blot analysis was used to detect cytochrome c release and apoptosis-related proteins. Transmission electron microscopy (TEM) was used to observe mitochondrial morphology. Cell viability significantly decreased and apoptosis significantly increased in SH-SY5Y cells treated with Aβ25–35, and both effects were rescued by NSC-CDM. In addition, NSC-CDM reduced ROS production and significantly inhibited the reduction of MMP caused by Aβ25–35. Furthermore, NSC-CDM ameliorated Aβ25–35-induced reduction in Bcl-2 expression levels and increased the expression levels of cytochrome c, caspase-9, caspase-3, and Bax. Moreover, Aβ25–35 induced the destruction of mitochondrial ultrastructure and this effect was reversed by NSC-CDM. Collectively, our findings demonstrated the protective effect of NCS-CDM against Aβ25–35-induced SH-SY5Y cell damage and clarified the mechanism of action of Aβ25–35 in terms of mitochondrial maintenance and mitochondria-associated apoptosis signaling pathways, thus providing a theoretical basis for the development of novel anti-AD treatments.

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“…In addition, the protective effect of ischemic postconditioning is comparable with that of IP. On the other hand, accumulating evidence has shown that drug treatments for ischemic myocardium at the onset of reperfusion (e.g., pharmacological postconditioning) are capable of providing a similar protective effect with ischemic postconditioning [6-9]. Pharmacological postconditioning represents an ideal alternative for ischemic postconditioning since its clinical operation is simpler than ischemic postconditioning.…”

Section: Introductionmentioning

confidence: 99%

ω-3 Polyunsaturated Fatty Acid Postconditioning Protects the Isolated Perfused Rat Heart from Ischemia-Reperfusion Injury

et al. 2018

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Aims: This study aimed to evaluate the cardioprotective effects of ω-3 polyunsaturated fatty acids (PUFAs) postconditioning against ischemia-reperfusion (I/R) injury. Methods: Sixty Sprague-Dawley rats were randomly divided into 4 groups (n = 15 for each) and used to generate the Langendorff isolated perfused rat heart model. The sham group received a continuous perfusion of 150 min. The remaining three I/R-treated groups sequentially received a 30-min perfusion, a 30-min cardioplegia, and a 90-min reperfusion. The I/R-ischemic preconditioning (IP) group additionally received three cycles of 20-s reperfusion and 20-s coronary reocclusion preceded the 90 min of reperfusion. The I/R-ω group were perfused with ω-3 PUFAs for 15 min before the 90 min of reperfusion. The myocardial infarct size, the degree of mitochondrial damage, the antioxidant capacity of the myocardium, and the cardiac functions during reperfusion were compared among groups. Results: Compared with the I/R group, the I/R-ω group had significantly reduced myocardial infarct size, reduced levels of lactate dehydrogenase and malondialdehyde, elevated superoxide dismutase level, and elevated rising (+dp/dt_max) and descending (–dp/dt_max) rate of left ventricular pressure. The I/R-ω group had a significantly lower rate of mitochondrial damage in myocardial tissue compared with the I/R and I/R-IP groups. Conclusion: ω-3 PUFA postconditioning possesses good cardioprotective effects and may be developed into a therapeutic strategy for myocardial I/R injury.

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Effects of endomorphin-1 postconditioning on myocardial ischemia/reperfusion injury and myocardial cell apoptosis in a rat model

Cited by 23 publications

References 30 publications

3,3′-Diindolylmethane attenuates cardiomyocyte hypoxia by modulating autophagy in H9c2 cells

3,3′-Diindolylmethane attenuates cardiomyocyte hypoxia by modulating autophagy in H9c2 cells

Neural stem cell-conditioned medium ameliorates Aβ25–35-induced damage in SH-SY5Y cells by protecting mitochondrial function

ω-3 Polyunsaturated Fatty Acid Postconditioning Protects the Isolated Perfused Rat Heart from Ischemia-Reperfusion Injury

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