مقالات پذیرفته شده در پنجمین کنگره بین المللی زیست پزشکی
covid19 and bradykinin storm
covid19 and bradykinin storm
AmirHosein Yari,1,*Anahita Samadzadeh,2Zahra Ebadi,3
1. Department of Biology, Faculty of Microbiology, Tabriz Branch, Islamic Azad University, Tabriz, Iran 2. Department of biology, Faculty of Basic Sciences, University of Maragheh, Maragheh, Iran. 3. Department of biology, Faculty of Basic Sciences, Azarbaijan Shahid Madani University, Tabriz, Iran
Introduction: Since December 2019, the Novel Coronavirus, commonly known as COVID-19, has been spreading across the globe. It poses a major danger to the community healthcare systems of every country on Earth. Despite the fact that the influenza pandemic began in 1918, Coronavirus illness 2019 has emerged as the most serious public health epidemic to have occurred since that time. The need of learning more about COVID-19's characteristics and interactions with human host cells cannot be overstated in order to develop effective COVID-19 treatments. Despite the fact that the severity of COVD-19 illness varies from patient to patient, the vast majority of them suffer from typical cold symptoms that develop to moderate Pneumonia. The presence of spike glycoproteins on the virus's envelope gives it a crown-like appearance under an electron microscope (corona is the Latin word for crown). Patients with moderate illness recover within a week, whereas those with severe disease have significant respiratory difficulties as a result of alveolar destruction, which ultimately results in mortality, particularly in the elderly with pre-existing diseases. Patients with moderate illness recover within a week, whereas those with severe disease have significant respiratory difficulties as a result of alveolar destruction, which ultimately results in mortality, particularly in the elderly with pre-existing diseases. Numerous polypeptides have been shown to have an effect on the smooth muscle of blood arteries. Oxytocin, vasopressin, angiotensin, anaphylatoxin, leucotaxine, and bradykinin are a few examples ( plasma kinin ) Brady kinin is one of the most obscure of these compounds. Bradykinin is formed when factor XII, prekallikrein, and high-molecular-weight kininogen interact with negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or when they clump together on the surface of cells. Bradykinin binds to endothelial B1 and B2 receptors and exerts a variety of pharmacological and physiological effects, including reduced blood pressure, increased vascular permeability, and stimulation of typical inflammatory symptoms such as vasodilation, heat, oedema, and pain. The virus enters the body via the protein ACE2, which is a component of the RAS hypotensive axis that works to prevent hypertension. It is a powerful component of the vasopressor system that causes hypotension and vasodilation.
Methods: Bradykinin is destroyed by ACE and increased by the angiotensin1-9 generated by ACE2. Earlier research has shown that bradykinin produces pain and causes blood vessels to dilate and leak, As a consequence, the surrounding tissue becomes swollen and inflamed. The analysis revealed a rise in the synthesis of a chemical called hyaluronic acid and a significant reduction in the enzymes capable of degrading it. Hyaluronic acid is capable of absorbing 1,000 times its own weight in water and forming a hydrogel. Bradykinin-Storm-induced fluid leaking into the lungs, coupled with an excess of hyaluronic acid, would likely result in a Jello-like material that prevents oxygen absorption and carbon dioxide release in the lungs of seriously afflicted patients. Patients with COVID-19.
Results: Thus, Garvin et alresults .'s suggest that the Bradykinin Storm may be responsible for the more severe COVID-19 symptoms. Although considerable attention has been focused on the lungs because to the need for ventilator assistance in advanced illness, COVID-19 also affects the gut, liver, kidney, heart, brain, and eyes. Cardiovascular damage occurs in almost one-fifth of hospitalized patients. This may be caused directly by viral infection and is consistent with the high expression of the SARS-CoV-2 receptor ACE2 in cardiac tissue. COVID-19 has been implicated in neurological disease following an MRI examination of COVID-19-positive individuals with encephalopathy symptoms in France showed elevation in leptomeningeal spaces and bilateral frontotemporal hypoperfusion. which are associated with increased cerebral vascular permeability. Direct viral infection and kidney injury were also found, most notably in the proximal tubules.
Conclusion: These last two results are unsurprising in light of the increased expression of ACE2 in these tissues relative to other tissues. Recent study indicates that some traditional Chinese medicines (TCMs) have anti-inflammatory, anti-renin-angiotensin system (RAS)-mediated bradykinin storm (RBS), and antiviral properties. The snake-derived bradykinin-potentiating peptide (BPP-10c) significantly reduces angiotensin II levels by inhibiting ACE, increasing bradykinin-related effects on the bradykinin 2-receptor, and increasing nitric oxide-mediated effects, and thus may be the most effective option to consider when developing an anti-SARS-COV-2 drug.