Pavel Nazarov, Marina Kuznetsova, Marina Karakozova
{"title":"Multidrug resistance pumps as a keystone of bacterial resistance","authors":"Pavel Nazarov, Marina Kuznetsova, Marina Karakozova","doi":"10.55959/msu0137-0952-16-2022-77-4-215-223","DOIUrl":"https://doi.org/10.55959/msu0137-0952-16-2022-77-4-215-223","url":null,"abstract":"Antibiotic resistance is a global problem of modern medicine. A harbinger of the onset of the post-antibiotic era is the complexity and high cost of developing new antibiotics, as well as their ineffi ciency due to the rapidly developing resistance of bacteria. The cornerstone of bacterial protection against antibiotics are multidrug resistance pumps (MDR), which are involved in the formation of resistance to xenobiotics, the export of toxins, the maintenance of cellular homeostasis, the formation of biofilms and persistent cells. MDR pumps are the basis for the nonspecific protection of bacteria, while modification of the drug target, inactivation of the drug, switching of the target or sequestration of the target is the second, specific line of their protection. Thus, the nonspecific protection of bacteria formed by MDR pumps is a barrier that prevents the penetration of antibacterial substances into the cell, which is the main factor determining the resistance of bacteria. Understanding the mechanisms of MDR pumps and a balanced assessment of their contribution to overall resistance, as well as to antibiotic sensitivity, will either seriously delay the onset of the post-antibiotic era, or prevent its onset in the foreseeable future","PeriodicalId":493507,"journal":{"name":"Vestnik Moskovskogo universiteta Seria 16 Biologia","volume":"164 2","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135834418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"CXCL12 mRNA expression as an independent marker of liver fi brogenesis in rats","authors":"E.I. Lebedeva, A.S. Babenka, A.Т. Shchastny","doi":"10.55959/msu0137-0952-16-2022-77-4-248-257","DOIUrl":"https://doi.org/10.55959/msu0137-0952-16-2022-77-4-248-257","url":null,"abstract":"The accumulated knowledge about the role of the CXCL12 chemokine in the initiation and development of liver fi brosis is insignifi cant and does not allow us to assess the potential of using the CXCL12 mRNA level as an independent marker of fi brogenesis and processes associated with fi brosis and cirrhosis. Thioacetamide modeling of liver fi brosis and cirrhosis in male Wistar rats showed a low level of CXCL12 mRNA expression (p = 0.0000) at all stages of fi brosis progression. At the beginning of the experiment (3 weeks), a decrease in the level of CXCL12 mRNA by 2.93 times (p = 0.0000) compared with the control group was revealed. After 3, 7 and 9 weeks, the level of gene expression decreased gradually (p = 0.0000). During the reorganization of the parenchyma of the organ and the formation of false hepatic nodules (11, 13 and 15 weeks), a certain stabilization of the level of gene expression was noted. Against the background of the total formation of pseudohepatic nodules and a pronounced diff use proliferation of connective tissue (17 weeks), the level of CXCL12 mRNA expression increased, but did not reach the level of control values. Based on our results, the level of CXCL12 mRNA is associated with the processes of fi brosis/cirrhosis and can act as an independent marker of fi brogenesis, but not cirrhosis of the liver against the background of toxic damage to it by thioacetamide. When conducting fundamental and preclinical studies to evaluate the eff ectiveness of drugs using this experimental model, the minimum allowable number of control points is considered to be three, namely: portal fi brosis (3 weeks), bridging fi brosis (5 weeks), the beginning of the process of transformation of liver fi brosis into cirrhosis (9 weeks).","PeriodicalId":493507,"journal":{"name":"Vestnik Moskovskogo universiteta Seria 16 Biologia","volume":"42 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135834411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}