Approaches for reducing chemo/radiation-induced cardiotoxicity by nanoparticles.

Nanoparticles are fascinating and encouraging carriers for cancer treatment due to their extraordinary properties and potential applications in targeted drug delivery, treatment, and diagnosis. Experimental studies including in vitro and in vivo examinations show that nanoparticles can cause a revolution in different aspects of cancer therapy. Normal tissue toxicity and early and late consequences are the major limitations of cancer therapy by radiotherapy and chemotherapy. However, the delivery of drugs into tumors or reducing the accumulation of drugs in normal tissues can permit a more satisfactory response of malignancies to therapy with more inferior side effects. Cardiac toxicity is one of the major problems for chemotherapy and radiotherapy. Therefore, several experimental studies have been performed to minimize the degenerative impacts of cancer treatment on the heart and also enhance the influences of radiotherapy and chemotherapy agents in cancers. This review article emphasizes the benefits of nanoparticle-based drug delivery techniques, including minimizing the exposure of the heart to anticancer drugs, enhancing the accumulation of drugs in cancers, and expanding the effectiveness of radiotherapy. The article also discusses the challenges and problems accompanied with nanoparticle-based drug delivery techniques such as toxicity, which need to be addressed through further research. Moreover, the article emphasizes the importance of developing safe and effective nanoparticle-based therapies that can be translated into clinical practice.

Apoptosis and heart failure: The role of non-coding RNAs and exosomal non-coding RNAs.

Heart failure is a condition that affects the cardio vascular system and occurs if the heart cannot adequately pump the oxygen and blood to the body. Myocardial infarction, reperfusion injury, and this disease is the only a few examples of the numerous cardiovascular illnesses that are impacted by the closely controlled cell deletion process known as apoptosis. Attention has been paid to the creation of alternative diagnostic and treatment modalities for the condition. Recent evidences have shown that some non-coding RNAs (ncRNAs) influence the stability of proteins, control of transcription factors, and HF apoptosis through a variety of methods. Exosomes make a significant paracrine contribution to the regulation of illnesses as well as to the communication between nearby and distant organs. However, it has not yet been determined whether exosomes regulate the cardiomyocyte-tumor cell interaction in ischemia HF to limit the vulnerability of malignancy to ferroptosis. Here, we list the numerous ncRNAs in HF that are connected to apoptosis. In addition, we emphasize the significance of exosomal ncRNAs in the HF.

Effect of Tegretol on Oxidative Stress, Serum Inflammatory Factors, and Left Ventricular Function in AMI Patients after Emergency PCI.

To investigate the effects of tegretol on oxidative stress, serum inflammatory factors, and left ventricular function in patients with acute myocardial infarction (AMI) after emergency percutaneous coronary intervention (PCI), 70 AMI patients who received PCI in the emergency department of our hospital from January 2021 to December 2021 were collected. The patients in the control group were treated with aspirin, clopidogrel, and heparin sodium during the perioperative period, and the patients in the study group were treated with tegretol. The levels of oxidative stress, serum inflammatory factors, and left ventricular function index were compared between the two groups. The patients in the control group were treated with TT ((12.00 ± 2.05) s), APTT ((35.50 ± 4.19) s), PT ((16.60 ± 1.58) s), TT ((15.90 ± 2.14) s) APTT ((30.40 ± 3.80) s), and PT ((14.30 ± 1.45) s)) and were comparable (P > 0.05), and the difference was statistically significant (t = 8.210, 4.600, 7.010, P < 0.001). There was no comparable difference in the level of oxidative stress index before treatment (P > 0.05). After treatment, there was significant difference in MDA ((14.53 ± 2.14) mmol/L), SOD ((120.45 ± 8.17) U/L), MDA ((11.15 ± 2.02) mmol/L), and SOD ((129.86 ± 8.55) U/L) in the control group (t = 7.320, 5.099, P < 0.001). The levels of inflammatory factors in patients before treatment were not comparable (P > 0.05). After treatment, there were levels of IL-6 ((3.20 ± 1.05) ng/L), CRP ((4.80 ± 1.16) mg/L), MPO ((196.78 ± 21.51) mg/L) and TNF-α ((3.96 ± 0.80) pmol/L), IL-6 ((1.95 ± 0.80) ng/L), CRP ((3.10 ± 1.02) mg/L), MPO ((163.60 ± 21.10) mg/L), and TNF-α in a study group level ((3.05 ± 0.70) pmol/L), with statistically significant difference (t = 5.187, 6.028, 6.031, 4.689,P < 0.001). Before treatment, there was no comparable difference in the level of left ventricular function index (P > 0.05). After treatment, there was significant difference in LVEF ((46.10 ± 2.39) %) and LVDD ((52.06 ± 1.07) mm), LVEF ((56.85 ± 2.33) %), and LVDD ((48.75 ± 1.02) mm) in the control group (t = 17.640, 21.540, P < 0.001). Tegretol as an adjunctive therapy for emergency PCI patients with acute myocardial infarction can effectively improve postoperative coagulation function, reduce oxidative stress and inflammatory reaction, and improve cardiac function indicators. It has a positive clinical value.

The relationship between phosphodiesterase 4D gene polymorphism and coronary heart disease.

Coronary atherosclerotic heart disease is one of the most common heart diseases that seriously endanger human health. The study found that intracellular second messenger CAMP plays an important role in inhibiting the proliferation and migration of vascular smooth muscle and the local inflammatory response at the damaged vessel. Phosphodiesterase 4D (PDE4D) can specifically degrade cAMP. The purpose of this article is to investigate the relationship between phosphodiesterase 4D gene polymorphism and coronary heart disease and the effect of phosphodiesterase 4D gene polymorphism on cardiovascular, using polymerase chain reaction-restriction fragment length polymorphism method (PCR-RFLP) was used to detect 50 patients with coronary heart disease (ACS group) and 100 patients who were diagnosed with coronary artery disease by coronary angiography at the same time as the control group (NC group). The results of the study showed that the frequencies of AA, AG, and GG genotypes in 150 samples were 25.67%, 54.66%, and 22.67%, respectively, which was consistent with Hard Weber's law (X = 2.186, P = 0.101). The distribution of GG genotype (18% vs. 27%), AA + AG genotype (85% vs. 74%), G (57% vs. 55%), A (43% vs. 45 %) There was no statistically significant difference in allele frequency (P <0.05). From this, it can be seen that the rs918592 polymorphism of the PDE4D gene is not associated with coronary heart disease.

Celastrol mitigates high glucose-induced inflammation and apoptosis in rat H9c2 cardiomyocytes via miR-345-5p/growth arrest-specific 6.

BACKGROUND: Celastrol (Cel) has been corroborated as an anti-inflammatory and anti-apoptotic agent in multiple cell damage models. However, the protective effect of Cel in high glucose (HG)-induced cardiomyocyte injury is still unclear. The present study aimed to determine whether Cel can mitigate HG-stimulated cardiomyocyte injury via regulating the miR-345-5p/growth arrest-specific 6 (Gas6) signaling pathway. METHODS: Cardiomyocytes were exposed to normal glucose (NG; 5 mmol/l) or HG (30 mmol/l) and then administered with Cel. Cell counting kit-8 and flow cytometry assays were used to detect cell proliferative activity and apoptosis. mRNA and protein expression were analyzed using a quantitative reverse transcriptase-polymerase chain reaction and western blotting, respectively. A bioinformatics algorithm and a luciferase reporter gene assay were used to determine whether Gas6 is a direct target of miR-345-5p. RESULTS: The present study confirmed the inhibitory effects of Cel in HG-induced inflammation in cardiomyocytes. Moreover, Cel exhibited the ability to antagonize HG-induced cardiomyocyte apoptosis and suppress the elevated Bax/Bcl-2 ratio elicited by HG stimulation. Intriguingly, Cel treatment revoked the HG-triggered repression of Gas6 protein expression, and Gas6 loss-of-function accelerated HG-induced cardiomyocyte apoptosis. HG-triggered up-regulation of miR-345-5p expression was depressed following Cel treatment. Importantly, we validated that Gas6 is a direct target of miR-345-5p. Transfection with miR-345-5p inhibitors restrained HG-induced release of pro-inflammatory cytokines and cell apoptosis. CONCLUSIONS: The findings of the present study demonstrate that Cel administration antagonized HG-induced cardiomyocyte apoptosis and inflammation through up-regulating Gas6 expression by restraining miR-345-5p.