Impact of COVID-19 on the Cardiovascular System: A Review of Available Reports.

The recent emergence of the coronavirus disease 19 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in China is now a global health emergency. The transmission of SARS-CoV-2 is mainly via human-to-human contact. This virus is expected to be of zoonotic origin and has a high genome identity to that of bat derived SARS-like coronavirus. Various stringent measures have been implemented to lower person-to-person transmission of COVID-19. Particular observations and attempts have been made to reduce transmission in vulnerable populations, including older adults, children, and healthcare providers. This novel CoV enters the cells through the angiotensin-converting enzyme 2 (ACE2) receptor. There is a higher risk of COVID-19 infection among those with preexisting cardiovascular diseases (CVD), and it has been connected with various direct and indirect complications, including myocarditis, acute myocardial injury, venous thromboembolism, and arrhythmias. This article summarizes the various cardiovascular complications and mechanisms responsible for the same with COVID-19 infection. For the benefit of the scientific community and public, the effect of COVID-19 on major vital organs such as the kidneys, liver, and intestines has been briefly discussed. In this review, we also discuss drugs in different stages of clinical trials and their associated complications, as well as the details of vaccines in various stages of development.

Passiflora edulis (var. Flavicarpa) Juice Supplementation Mitigates Isoproterenol-induced Myocardial Infarction in Rats.

The common reason for mortality globally is myocardial infarction. The study aimed to evaluate Passiflora edulis (PE) fruit juice potential in the experimental isoproterenol (ISO) treated rat model to manage myocardial injury. ISO (20 mg/100 g body weight) treated rats showed a significant increment in serum marker enzymes lactate dehydrogenase (LDH) and creatinine kinase (CK), serum glutamate pyruvate transaminase (SGPT), serum glutamate oxaloacetate transaminase (SGOT), serum alkaline phosphatase (ALP) and serum acid phosphatase (ACP) activity. Besides, phosphorus and calcium, serum cholesterol, and triglyceride levels (TG) were high in ISO groups. A significant decline in antioxidant activity and histopathological alteration was observed in ISO treated groups. PE juice pre-treatment (2 ml/kg) for 28 days and ISO treatment on the 29th and 30th days showed a protective effect on distorted biochemical and histopathologic parameters compared with reference drug metoprolol. These findings indicate the cardioprotective effect of PE juice on ISO-induced myocardial infracted rats.

Allicin functionalized locust bean gum nanoparticles for improved therapeutic efficacy: An in silico, in vitro and in vivo approach.

The field of nanotechnology has overgrown over the past few years and has even ventured into the field of medicine. The aim of the present study is to develop a novel allicin functionalized locust bean gum nanoparticle using the nanoprecipitation technique. The synthesized nanoparticles were characterized by dynamic light scattering, scanning electron microscopy and transmission electron microscopy. The characterization study revealed the nanoscale structure (∼100nm) of the prepared particles. In silico toxicology analysis were carried out to assess the drug-like properties and virtual toxicity of allicin. Toxicity of the prepared nanoparticles were carried out in RAW 264.7 cell lines in vitro and in vivo studies were carried out in Sprague-Dawley rats. In in vitro study, LBGAN showed a maximum toxicity of 10.51% in MTT assay, no reactive oxygen species generation on DCFDA staining and LBGAN was effective to protect the cells from apoptosis. In in vivo toxicity studies LBGAN showed no significant change in the activities of the marker enzymes like LDH, CK-MB, ALP, ACP, AST and ALT. Thus, the functionalization of nanoparticles with allicin has the benefit of providing protection and stability to the allicin, in addition to increasing its pharmacological activity.

Selenium incorporated guar gum nanoparticles safeguard mitochondrial bioenergetics during ischemia reperfusion injury in H9c2 cardiac cells.

The application of nanotechnology has created high impact in diagnosis and prognosis of various disorders including cardiovascular diseases. In the present study, we investigated the beneficial effect of selenium incorporated guar gum nanoparticles (SGG) compared to nascent selenium (Se) and guar gum nanoparticles (GGN) against ischemiareperfusion (IR) induced alterations in oxidative phosphorylation and energy metabolism in H9c2 cardiac cells. Ischemia and reperfusion were induced for 1h. The alterations in activities of various complexes (complex 1, II, III and IV) of mitochondrial electron transport chain (ETC), aconitase activity, oxygen consumption rate, and the ATP content were seen. The role of heat shock protein, hypoxia inducible factor-1α and atrial natriuretic factor (ANP) were also analyzed. Then the beneficial properties of various particles like Se, GGN and SGG were evaluated. Among these, SGG treatment (1 and 5ng) was found to be more beneficial compared to other particles. Overall results reveal that SGG nanoparticles are effective in protecting H9c2 cardiac cells from IR injury via improving the efficiency of ETC in H9c2 cells.

Beneficial properties of selenium incorporated guar gum nanoparticles against ischemia/reperfusion in cardiomyoblasts (H9c2).

Nanotechnology for the treatment and diagnosis has been emerging recently as a potential area of research and development. In the present study, selenium incorporated guar gum nanoparticles have been prepared by nanoprecipitation and characterized by transmission electron microscopy and particle size analysis. The nanoparticles were screened for antioxidant potential (metal chelation, total reducing power and hydroxyl radical scavenging activity) and were evaluated against the cell line based cardiac ischemia/reperfusion model with special emphasis on oxidative stress and mitochondrial parameters. The cell based cardiac ischemia model was employed using H9c2 cell lines. Investigations revealed that there was a significant alteration (P ≤ 0.05) in the innate antioxidant status (glutathione↓, glutathione peroxidase↓, thioredoxin reductase↓, superoxide dismutase↓, catalase↓, lipid peroxidation↑, protein carbonyl↑, xanthine oxidase↑ and caspase 3 activity↑), mitochondrial functions (reactive oxygen species generation, membrane potential, and pore opening) and calcium homeostasis (calcium ATPase and intracellular calcium overload) during both ischemia and reperfusion. For comparative evaluation, selenium, guar gum and selenium incorporated guar gum nanoparticles were evaluated for their protective properties against ischemia/reperfusion. The study reveals that selenium incorporated guar gum nanoparticles were better at protecting the cells from ischemia/reperfusion compared to selenium and guar gum nanoparticles. The potent antioxidant capability shown by the sample in in vitro assays may be the biochemical basis of its better biological activity. Further, the nanodimensions of the particle may be the additional factor responsible for its better effect.

Synthesis, characterization and evaluation of the antioxidant potential of vanadium encapsulated guar gum nanoparticles.

The present study investigated the antioxidant potential of guar gum macroparticles (GGMs), vanadium oxide sulphate (VS) encapsulated guar gum macroparticles (GVMs), guar gum nanoparticles (GGNs), VS encapsulated guar gum nanoparticles (GVNs) and VS. GGNs and GVNs prepared by nanoprecipitation were characterized by SEM (scanning electron microscopy), TEM (transmission electron microscopy) and particle size analysis to confirm the nanostructure of the particles. Particle size analysis revealed that GVNs possess a size of 239 nm, about 148 nm larger than that of GGNs. TEM imaging and EDAX data also confirmed the formation of fine spherical nanoparticles with vanadium incorporation. In addition the larger size of GVNs also confirmed the vanadium incorporation. MTT assay showed that concentrations up to 100 nM of GVNs for 24 h exposure did not induce significant toxicity when VS was toxic (16%) at 100 nM. Various in vitro antioxidant assays (total reducing power, total antioxidant capacity, DPPH (2,2-diphenyl-1-picrylhydrazyl), ABTS (2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid), hydroxyl radical and superoxide anion radical scavenging assays) revealed significantly high antioxidant potential of GVNs compared to GGNs, VS, GGMs and GVMs. The IC50 of GVNs was 23.21 ± 2.1 µg mL(-1), 33.0 ± 2.93 µg mL(-1), 21 ± 1.98 µg mL(-1) and 22.79 ± 2.12 µg mL(-1) for DPPH, ABTS, hydroxyl, superoxide anion scavenging activity assays respectively. The cell line based assay also proved that the GVN was more effective in reactive oxygen species (ROS) scavenging than VS against tertiary butyl hydrogen peroxide (TBHP) induced oxidative stress in H9c2 cell lines. The overall results indicated that vanadium in combination with nano guar gum exhibits significantly high antioxidant potential.

Arsenic trioxide toxicity in H9c2 myoblasts--damage to cell organelles and possible amelioration with Boerhavia diffusa.

Arsenic trioxide (ATO) has been long used as a chemotherapeutic agent because of its significant anticancer property. Unfortunately, the use of ATO is limited due to its cardiotoxic effects. The present study evaluates the protective property of ethanolic extract of Boerhavia diffusa (BDE) against ATO-induced toxicity on various cell organelles in H9c2 cardiomyocytes. The effects of different concentrations of ATO (5, 7.5 and 10 µM) on cell organelles like mitochondria, endoplasmic reticulum (ER), lysosome and actin, generation of reactive oxygen species, antioxidant enzyme status and intracellular calcium overload were evaluated. ATO significantly (P ≤ 0.05) altered mitochondrial transmembrane potential, intracellular calcium level, ER, lysosomal activity and F-actin network in addition to induction of oxidative stress. Co-treatment with BDE protected the cardiomyocytes from the adverse effects of ATO, especially at 5 µM concentration, which was evident from decreased activity of lactate dehydrogenase (5 µM ATO + 20 µg/mL BDE: 6.61 ± 1.97 µU/mL, respective control group: 16.15 ± 1.92 µU/mL), reduced oxidative stress, calcium influx and organelle damage. Results obtained from the present study allow for a better characterization of the effects of ATO on H9c2 myoblasts. In conclusion, our data suggest that cell organelles are also the targets of ATO-induced cardiotoxicity in addition to other reported targets like ion channels, and BDE has the potential to protect the cardiotoxicity induced by ATO.