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Cardiomyocytes Apoptosis - Europe PMC

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Last Updated: 13 July 2022

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Upregulation of miR-144-3p alleviates Doxorubicin-induced heart failure and cardiomyocytes apoptosis via SOCS2/PI3K/AKT axis.

Background MicroRNAs are often blamed for heart failure. Methods Doxorubicin-induced HF model was developed in rats and cardiomyocytes H9C2, and the cardiac function was determined using ultrasound cardiography. Using Cell Counting Kit-8 assay and flow cytometry, the viability and apoptosis of Dox-treated and transfected cardiomyocytes were determined. With dual-luciferase reporter assay, the target gene of miR-144-3p was both predicted and announced. Both PI3K and AKT's cardiac function, aggravated cardiac arrest, reduced cardiomyocytes' viability, and the expression of miR-144-3p, Bcl-2, and phosphorylation of both PI3K and AKT were reversed by upregulating miR-144-3p, while downregulating miR-144-3p reversed. MiR-144-3p was the target gene of miR-144-3p, which was reversed by upregulating miR-144-3p, while downregulating miR-144-3p did conversely, which was reversed by upregulating miR-144-3p. Conclusion MiR-144-3p in HF was able to resolve Dox-induced cardiac dysfunction and cell apoptosis by utilizing SOCS2, which gave the first evidence of miR-144-3p in HF.

Source link: https://europepmc.org/article/MED/35730258


MiR-19a-3p mitigates hypoxia/reoxygenation-induced apoptosis in H9C2 cardiomyocytes by targeting SOCS3

It's likely that the relationship between the I/R injury and miR-19a-3p is undetermined. In H9C2 cardiomyocytes, the role of miR-19a-3p in injuries caused by I/R was investigated. MiR-19a-3p inhibition prevented apoptosis caused by miR-19a-3p inhibition, causing apoptosis caused by miR-19a-3p inhibition, but SOCS3's overexpression prevented a miR-19a-3p mimic's effect on apoptosis. MiR-19a-3p reduces apoptosis and injury caused by H/R in cardiomyocytes by targeting SOCS3, and targeting miR-19a-3p/SOCS3 signalling may be a new approach in the treatment of myocardial I/R injury.

Source link: https://europepmc.org/article/PPR/PPR504717


Quercetin Mitigates Cisplatin-Induced Oxidative Damage and Apoptosis in Cardiomyocytes through Nrf2/HO-1 Signaling Pathway.

In patients receiving cisplatin, cardiotoxicity may result in congestive heart failure and even sudden cardiac death. Quercetin is a flavonol compound that can be found in dietary fruits and vegetables. However, it is also unknown if quercetin will shield against cisplatin-caused apoptosis and cell damage in cardiomyocytes. Myocytes were treated with cisplatin for 24 hours to cause cellular damage, with or without quercetin pretreatment. Quercetin stimulates Nrf2 and HO-1 expression in H9c2 cells, thus reducing cisplatin-caused cytotoxicity in H9c2 cells. Quercetin also raises SOD levels, maintains mitochondrial function, and reduces oxidative stress under cisplatin stimulation. p38MAPK/NF/NF signaling pathway [Formula]Bp65/IL-8 signaling pathway In conclusion, this research shows that quercetin has the ability to antagonize cisplatin-caused cardiotoxicity by reducing ROS-mediated mitochondrial damage and inflammation via the Nrf2/HO-1 and NF-[Formula: see text] Bp65/IL-8 signaling pathway. This review provided both the theoretical foundation and experimental evidence for quercetin's clinical use as a novel safe way to treat chemotherapy-induced cardiotoxicity.

Source link: https://europepmc.org/article/MED/35670059


Hydroxytyrosol Prevents Doxorubicin-Induced Oxidative Stress and Apoptosis in Cardiomyocytes.

Doxorubicin, a highly effective chemotherapeutic agent used in the treatment of hematologic and solid tumors, is a very strong chemotherapeutic agent. Due to Dox's well-known cardiotoxic side effects, mainly due to oxidative damage, its use in cancer therapy has been severely limited. Plant polyphenols have attracted considerable attention due to their antioxidant properties and excellent safety profile, and hydroxytyrosol, the most common phenolic compound in olive oil, may be a potential candidate due to its unique antioxidant and anticancer properties. Using a combination of biochemical and cellular biology methods, the effect of HT on Dox-induced cardiotoxicity was investigated in this research. Interestingly, HT was able to counteract Dox-induced cytotoxicity in cardiomyocytes by focusing on the SOD2 level and the oxidative response, as well as a Bcl-2/Bax's apoptotic pathways. HT did not want to interfere with Dox's antitumorigenic characteristics in osteosarcoma cells at the same time, but did not want to influence the antitumorigenic properties of osteosarcoma cells.

Source link: https://europepmc.org/article/MED/35739984


Mesenchymal Stem Cell-Originated Exosomal Lnc A2M-AS1 Alleviates Hypoxia/Reperfusion-Induced Apoptosis and Oxidative Stress in Cardiomyocytes.

Long-coding RNA alpha-2-macroglobulin antisense RNA 1 was discovered that could shield against myocardial I/R. However, it is also unknown if Lnc A2M-AS1 delivery by MSC-derived exosomes could also control myocardial I/R injury. In vitro, hypoxia/reoxygenation therapy in human cardiomyocytes was used to mimic the process of myocardial I/R in vitro. The dual-luciferase reporter, RIP and pull-down assays, confirmed the binding relationship between miR-556-5p and Lnc A2M-AS1 or XIAP. In AMI patients and H/R-induced cardiomyocytes, Lnc A2M-AS1 was poorly expressed in AMI patients and H/R-induced cardiomyocytes. Besides, Lnc A2M-AS1-transfected hMSCs-exo, exosomes derived from Lnc A2M-AS1-infected hMSCs, weakened H/R-induced apoptosis and oxidative stress, as well as an improved protection of hMSCs-exo, which also improved the protective action of hMSCs-exo on heartmyocytes. Lnc A2M-AS1 was used as a sponge for miR-556-5p to raise XIAP expression level by a further mechanism review.

Source link: https://europepmc.org/article/MED/35543792


Saprirearine protects H9c2 cardiomyocytes against hypoxia/reoxygenation-induced apoptosis by activating Nrf2.

Myocardial infarction is a leading cause of mortality and disability around the world. Saprirearine improved cell viability while also blocking the release of lactate dehydrogenase, according to the study. Saprirearine was found to reduce mitochondrial dysfunction by blocking calcium depletion, mitochondrial membrane degeneration, and the opening of the mitochondrial transition pore. In addition, saprirearine inhibited cysteinyl aspartate-specific proteinase-3, the up-regulated B-cell lymphoma-2 and down-regulated Bcl-2-associated X protein, to reduce hypoxia/reoxygenation-induced apoptosis, leading to hypoxia/reoxygenation-induced apoptosis. A2-related factor-2 in H9c2 cardiomyocytes has been identified as closely related to its protective properties, according to further research, saprirearine-activated nuclear factor E2-related factor-2, which is closely linked to its protective functions.

Source link: https://europepmc.org/article/MED/35617158

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions