Garasiya A Ajitbhai, Prati P Singh, Mukesh Kumar, Rajinder Singh, Vandana Dhiman
{"title":"deltorphin-II 对受疟原虫感染的小鼠疟疾发展的抑制作用。","authors":"Garasiya A Ajitbhai, Prati P Singh, Mukesh Kumar, Rajinder Singh, Vandana Dhiman","doi":"10.5281/zenodo.10870022","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Drug resistance has been one of the main obstacles in the fight against vector-borne infectious diseases. Among these diseases, malaria represents a serious public health challenge, mainly in the tropics, where vector-favourable climates are a crucial factor. Each of the various anti-malarial drugs currently used against this disease, such as quinolones, sulphonamides and artemisinins are inadequate and new strategies are required. Peptides are known to have a huge number of biological effects. Antimicrobial peptides (AMPs) have been proven to be effective against bacterial, fungal and viral infections. This study explored the effect of the peptide 'deltorphin-II' in <i>Plasmodium berghei-</i>infected mice.</p><p><strong>Materials and methods: </strong>Mean percentage parasitaemia was calculated by studying infected erythrocytes after microscopic examination of 10<sup>4</sup> erythrocytes from infected mice on days 4, 7, 10, 14 and 21 after infection in all groups. <b>Results.</b> Deltorphin-II shows maximum activity at a dose of 0.8 mg/kg/day from day 4 to day 21. Pre-treatment of infected mice with naltriben abrogates the deltorphin-II-mediated effect.</p><p><strong>Conclusion: </strong>Deltorphin-II inhibits the development of malaria, most probably via activation of the δ<sub>2</sub> receptor.</p>","PeriodicalId":74100,"journal":{"name":"MalariaWorld journal","volume":"6 ","pages":"3"},"PeriodicalIF":0.0000,"publicationDate":"2015-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11107872/pdf/","citationCount":"0","resultStr":"{\"title\":\"Inhibitory effect of deltorphin-II on development of malaria in <i>Plasmodium berghei</i>-infected mice.\",\"authors\":\"Garasiya A Ajitbhai, Prati P Singh, Mukesh Kumar, Rajinder Singh, Vandana Dhiman\",\"doi\":\"10.5281/zenodo.10870022\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Drug resistance has been one of the main obstacles in the fight against vector-borne infectious diseases. Among these diseases, malaria represents a serious public health challenge, mainly in the tropics, where vector-favourable climates are a crucial factor. Each of the various anti-malarial drugs currently used against this disease, such as quinolones, sulphonamides and artemisinins are inadequate and new strategies are required. Peptides are known to have a huge number of biological effects. Antimicrobial peptides (AMPs) have been proven to be effective against bacterial, fungal and viral infections. This study explored the effect of the peptide 'deltorphin-II' in <i>Plasmodium berghei-</i>infected mice.</p><p><strong>Materials and methods: </strong>Mean percentage parasitaemia was calculated by studying infected erythrocytes after microscopic examination of 10<sup>4</sup> erythrocytes from infected mice on days 4, 7, 10, 14 and 21 after infection in all groups. <b>Results.</b> Deltorphin-II shows maximum activity at a dose of 0.8 mg/kg/day from day 4 to day 21. Pre-treatment of infected mice with naltriben abrogates the deltorphin-II-mediated effect.</p><p><strong>Conclusion: </strong>Deltorphin-II inhibits the development of malaria, most probably via activation of the δ<sub>2</sub> receptor.</p>\",\"PeriodicalId\":74100,\"journal\":{\"name\":\"MalariaWorld journal\",\"volume\":\"6 \",\"pages\":\"3\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2015-03-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11107872/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"MalariaWorld journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5281/zenodo.10870022\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2015/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"MalariaWorld journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5281/zenodo.10870022","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2015/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
Inhibitory effect of deltorphin-II on development of malaria in Plasmodium berghei-infected mice.
Background: Drug resistance has been one of the main obstacles in the fight against vector-borne infectious diseases. Among these diseases, malaria represents a serious public health challenge, mainly in the tropics, where vector-favourable climates are a crucial factor. Each of the various anti-malarial drugs currently used against this disease, such as quinolones, sulphonamides and artemisinins are inadequate and new strategies are required. Peptides are known to have a huge number of biological effects. Antimicrobial peptides (AMPs) have been proven to be effective against bacterial, fungal and viral infections. This study explored the effect of the peptide 'deltorphin-II' in Plasmodium berghei-infected mice.
Materials and methods: Mean percentage parasitaemia was calculated by studying infected erythrocytes after microscopic examination of 104 erythrocytes from infected mice on days 4, 7, 10, 14 and 21 after infection in all groups. Results. Deltorphin-II shows maximum activity at a dose of 0.8 mg/kg/day from day 4 to day 21. Pre-treatment of infected mice with naltriben abrogates the deltorphin-II-mediated effect.
Conclusion: Deltorphin-II inhibits the development of malaria, most probably via activation of the δ2 receptor.