动物造模,新冠病毒感染 z-bio 2021-11-06 399

　　In a recent study, researchers at the University of São Paulo (USP) in Brazil discovered that melatonin synthesized in the lungs may act as a barrier to SARS-CoV-2 and prevent the expression of genes that contribute to virus invasion. Therefore, melatonin prevents the virus from infecting these cells and suppresses the immune response. This finding helps to understand why some people are not infected with COVID-19 or show symptoms of COVID-19 even if they are not diagnosed by RT-PCR. The results of an article published by researchers in Melatonin Research emphasized the need for preclinical and clinical trials to prove the antiviral efficacy of melatonin. Professor of USP Institute, Article author Regina Pekelmann Markus said: "We have shown that the melatonin produced in the lungs can act as a barrier to SARS-CoV-2, which can prevent the virus from invading the epithelium, activate the immune system and induce antibody production. Melatonin in the lungs This mechanism of action also includes other respiratory diseases.

　　 Marcus began researching melatonin in the 1990s. In a study of rodents, she found that the hormones produced by the pineal gland in the brain at night can tell organisms that sunlight has disappeared and they need to prepare for sleep. In addition to the brain, this hormone can also be produced in other organs, such as the lungs. In one involving In rodent studies, Marcus and colleagues found that macrophages in the lungs swallow contaminated particles, which further stimulated macrophages to produce melatonin and other molecules, which stimulated mucus formation, coughing and sputum. liquid. Exhaust particles from the respiratory tract. Researchers have observed that when the synthesis of melatonin in macrophages is blocked, contaminated particles enter the blood, spread throughout the organism, and even invade the brain. Based on the discovery that melatonin produced in the lungs changed the entry of particulate matter in air pollution, Markus and his collaborators asked whether hormones have the same function in SARS-CoV-2, and I decided to investigate. "In this case, the virus cannot bind to the ACE-2 receptor on the cell, enter the epithelium and infect the organism." In order to test this hypothesis, the researchers wrote 455 in the literature and COVID, and I did it. analysis. -19 Genes related to complications, the interaction between SARS-CoV-2 and human proteins, and the entry point of the virus. They selected 212 genes from this set of genes that are involved in viral cell invasion, intracellular transport, mitochondrial activity, and transcription and post-translational processes. They used RNA sequencing data downloaded from public databases to quantify the expression levels of 212 COVID-19 signature genes in 288 samples from healthy human lungs. Next, based on the analysis of the lungs of healthy rodents, the expression levels of these genes are correlated with the Gene Index (MEL-Index), which assesses the ability of the lungs to synthesize melatonin. They found that the lower the index, the higher the expression level of genes encoding proteins in macrophages and epithelial cells. This index is also negatively correlated with the protein gene of the modified cell receptor CD147 (viral entry point for macrophages and other immune cells), indicating that normal lung melatonin production may be a natural protective agent against viruses. Have.

　　"We found that a higher MEL index would close the entry point of the virus in the lungs, while a lower MEL index would open these "doors".