Background: New potential biological targets prediction through inverse molecular docking technique is an another smart strategy to forecast the possibility of compounds being biologically active against various target receptors. Objectives: In this case of designed study, we screened our recently obtained novel acetylinic steroidal biotransformed products [(1) 8-β-methyl-14-α-hydroxy∆4tibolone (2) 9-α-Hydroxy∆4 tibolone (3) 8-β-methyl-11-β-hydroxy∆4tibolone (4) 6-β-hydroxy∆4tibolone, (5) 6-β-9-α-dihydroxy∆4tibolone (6) 7-β-hydroxy∆4tibolone) ] from fungi Cunninghemella Blakesleana to predict their possible biological targets and profiling of ADME properties. Method: The prediction of pharmacokinetics properties membrane permeability as well as bioavailability radar properties were carried out by using Swiss target prediction, and Swiss ADME tools, respectively these metabolites were also subjected to predict the possible mechanism of action along with associated biological network pathways by using Reactome data-base. Results: All the six screened compounds possess excellent drug ability criteria, and exhibited exceptionally excellent non inhibitory potential against all five isozymes of CYP450 enzyme complex, including (CYP1A2, CYP2C19, CYP2C9, CYP2D6, and CYP3A4) respectively. All the screened compounds are lying within the acceptable pink zone of bioavailability radar and showing excellent descriptive properties. Compounds [1-4 & 6] are showing high BBB (Blood Brain Barrier) permeation, while compound 5 is exhibiting high HIA (Human Intestinal Absorption) property of (Egan Egg). Conclusion: In conclusion, the results of this study smartly reveals that in-silico based studies are considered to provide robustness towards a rational drug designing and development approach, therefore in this way it helps to avoid the possibility of failure of drug candidates in the later experimental stages of drug development phases.

Autoimmune thyroid illnesses are a category of disorders characterized by aberrant lymphocyte activity directed against self-tissues and are mostly represented by Hashimoto's thyroiditis and Graves' disease, which affect about 2% to 3% of the population, with a female predominance. Autoimmune thyroid disease is the most prevalent thyroid illness in children; the most typical age of onset is puberty, although the disease can strike at any age, including children as young as one-year-old. Autoantibodies to pendrin, an iodide transporter found at the apical pole of thyroid follicular cells, have recently been discovered in the majority of Hashimoto's thyroiditis and Graves' disease patients. Excessive iodine administration has been linked to an increased prevalence of thyroiditis in humans, according to recent epidemiologic research. People in North America consumed more than three times the recommended daily iodine intake. Antithyroglobulin antibody, anti-thyroperoxidase antibody, serum thyroid-stimulating hormone, and exacerbation of lymphocytic infiltration in the thyroid were all higher in these persons, indicating that iodine overconsumption could cause hypothyroidism and exacerbate the autoimmune response. However, the exact mechanism by which high iodine consumption causes autoimmune thyroid disease is yet unknown.

SARS CoV infection is one of the most common and economically damaging and life-threatening infections of the last 100 years. To combat it, first of all, it is necessary to study the mechanisms that stimulate its development. For this purpose, the role of genomic changes and oxidative stress in the spread of SARS-CoV virus is investigated. During the spread of this disease, lung damage has been found to occur under a "cytokine storm" caused by active forms of oxygen. SARS virus binds to target cells via angiotensin converting enzyme-2 (ACE2). In the early stages of the disease, SARS viruses cause accumulation and activation of NLRP3-inflammation, which plays a leading role in the formation of the inflammatory response to the virus. During the cytokine storm phase, interleukins, monocytic hematopoietic protein MCP-1, macrophage inflammatory protein MIP-1a, TGF, CCL2, CXCL10, CNXL9, TNF-a continue to increase. SARS-CoV-3b protein and nonstructural protein 10 (nsp10) of COVID virus in mitochondria It promotes the formation of OAF. 3CLpro protease is also known to cause apoptosis in human promonocytes by increasing OAF formation. Activation of the NF-κB transcription factor through oxidative stress can lead to severe lung damage. Naturally, in response to oxidative stress, the antioxidant system is activated, resulting in the depletion of the enzymatic and non-enzymatic branches of the system. After acquaintance with this mechanism, the reason for the spread of SARS COV infection in patients with hypertension treated with ACE-2 blockers is known. The therapeutic effect of antioxidants in this disease is also accepted as an undeniable fact. Key words: SARS-CoV, cytokine storm, oxidative stress SARS-COV infeksiyasının yayılmasında Sitokin Fırtınasının və Oksidativ Stressin rolu Xülasə SARS CoV infeksiyası son 100 ilin ən çox yayılmış və iqtisadi cəhətdən zərərli və həyati təhlükəsi olan infeksiyalardan biridir. Bununla mübarizə aparmaq üçün ilk növbədə onun inkişafını stimullaşdıran mexanizmləri öyrənmək lazımdır. Bu məqsədlə SARS-CoV virusunun yayılmasında genomik dəyişikliklərin və oksidləşdirici stressin rolu araşdırılır. Bu xəstəliyin yayılması zamanı oksigenin aktiv formalarının yaratdığı “sitokin fırtınası” altında ağciyər zədələnməsinin baş verdiyi aşkar edilmişdir. SARS virusu angiotenzin çevirən ferment-2 (ACE2) vasitəsilə hədəf hüceyrələrə bağlanır. Xəstəliyin erkən mərhələlərində SARS virusları NLRP3-iltihabın yığılmasına və aktivləşməsinə səbəb olur, virusa qarşı iltihablı reaksiyanın formalaşmasında aparıcı rol oynayır. Sitokin fırtınası mərhələsində interleykinlər, monositik hematopoetik protein MCP-1, makrofaq iltihablı protein MIP-1a, TGF, CCL2, CXCL10, CNXL9, TNF-a artmağa davam edir. Mitoxondriyadakı SARS-CoV-3b zülalı və qeyri-struktur protein 10 (nsp10) COVID virusu OAF-nin əmələ gəlməsini təşviq edir. 3CLpro proteazının OAF əmələ gəlməsini artıraraq insan promonositlərində apoptoza səbəb olduğu da məlumdur. NF-κB transkripsiya faktorunun oksidləşdirici stress vasitəsilə aktivləşdirilməsi ağciyərin ciddi zədələnməsinə səbəb ola bilər. Təbii ki, oksidləşdirici stressə cavab olaraq antioksidant sistem aktivləşir, nəticədə sistemin fermentativ və qeyri-fermentik şaxələri tükənir. Bu mexanizmlə tanışlıqdan sonra ACE-2 blokerləri ilə müalicə olunan hipertansiyonlu xəstələrdə SARS COV infeksiyasının yayılmasının səbəbi məlumdur. Bu xəstəlikdə antioksidantların müalicəvi təsiri də danılmaz fakt kimi qəbul edilir. Açar sözlər: SARS-CoV, sitokin fırtınası, oksidləşdirici stress

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The purpose of the study is to elucidate the interrelationships and notable correlations among the indicators of hormonal regulation, immune status, and markers of neurodegeneration in patients diagnosed with autoimmune thyroiditis. The study enrolled a total of 170 patients with autoimmune thyroiditis (divided subclinical and manifest form). Control group consist of 65 people without thyroid pathologies or other autoimmune diseases. The examination of cytokine profiles in patients with autoimmune thyroiditis revealed a significant increase in cytokine levels in groups of patients with subclinical and manifest forms of the disease compared to the control group. The analysis of antibody levels in patients with different clinical forms of hypothyroidism revealed that the median concentration of Ab-nDNA was significantly higher in patients with a manifest form of the disease compared to those with a subclinical group. According to an assessment of neuron-spesific enolase levels in the blood plasma of patients with autoimmune thyroiditis significantly compared to control group. Furthermore, a study examining the concentration of neuron-spesific enolase in patients with different clinical forms of autoimmune thyroiditis revealed that individuals with a subclinical form of the disease had statistically significant increase (p=0.042) in the value of this parameter. Our study results revealed significant changes in immunological parameters and markers of neurodegeneration in patients with autoimmune thyroiditis alongside hormonal imbalance.