Anti-Inflammatory Properties of Drugs Used to Control COVID-19 and their Effects on the Renin-Angiotensin System and Angiotensin-Converting Enzyme-2.
Identifieur interne : 001024 ( Main/Corpus ); précédent : 001023; suivant : 001025Anti-Inflammatory Properties of Drugs Used to Control COVID-19 and their Effects on the Renin-Angiotensin System and Angiotensin-Converting Enzyme-2.
Auteurs : Hamed Gilzad-Kohan ; Fakhreddin JamaliSource :
- Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques [ 1482-1826 ] ; 2020.
English descriptors
- KwdEn :
- Angiotensin-Converting Enzyme 2 (MeSH), Anti-Inflammatory Agents (administration & dosage), Anti-Inflammatory Agents (pharmacology), Antiviral Agents (administration & dosage), Antiviral Agents (pharmacology), COVID-19 (MeSH), Coronavirus Infections (drug therapy), Coronavirus Infections (virology), Humans (MeSH), Inflammation (drug therapy), Inflammation (virology), Pandemics (MeSH), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (drug therapy), Pneumonia, Viral (virology), Renin-Angiotensin System (drug effects).
- MESH :
- chemical , administration & dosage : Anti-Inflammatory Agents, Antiviral Agents.
- chemical , metabolism : Peptidyl-Dipeptidase A.
- chemical , pharmacology : Anti-Inflammatory Agents, Antiviral Agents.
- chemical : Angiotensin-Converting Enzyme 2.
- drug effects : Renin-Angiotensin System.
- drug therapy : Coronavirus Infections, Inflammation, Pneumonia, Viral.
- virology : Coronavirus Infections, Inflammation, Pneumonia, Viral.
- COVID-19, Humans, Pandemics.
Abstract
COVID-19 infection is associated with systemic inflammation, and sometimes hyperinflammatory responses with cytokine storm. This plays a major role in COVID-19 severity and poor disease prognosis, even death. Higher levels of inflammatory hallmarks including C-reactive protein, ferritin, D-dimers, and cytokines such as interleukin (IL) -6, IL-10 and tumor necrosis factor- α (TNF-α) have been reported. Many anti-viral drugs have been tried, but none were proven fully effective. Supportive care and management of the complications that are caused mainly by inflammation might be the key to greater survival rates and shorter hospitalization (e.g., the use of remdesivir, lopinavir, ritonavir, umifenovir (arbidol), oseltamivir, ganciclovir, favipiravir, darunavir, hydroxychloroquine, chloroquine, colchicine, azithromycin, anakinra, canakinumab, tocilizumab, siltuximab, sarilumab, Type 1 interferon, interferon β-1a, interferon α- 2b, baricitinib, ruxolitinib, fedratinib, methylprednisolone and dexamethasone). However, the efficacy of these treatments still needs well-planned clinical trials. In such trials, careful attention must be paid to the duration of the treatment, the onset of beneficial effects, and the severity of the disease, otherwise, the outcomes may still remain inconclusive. Herein, we present a review of the current drugs, which are being used in the management of the disease and their anti-inflammatory properties. We also investigated if these drugs directly interact with Angiotensin-Converting Enzyme (ACE 2), which is a crucial component of the virus entry to the cells.
DOI: 10.18433/jpps31346
PubMed: 32735768
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pubmed:32735768Le document en format XML
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This plays a major role in COVID-19 severity and poor disease prognosis, even death. Higher levels of inflammatory hallmarks including C-reactive protein, ferritin, D-dimers, and cytokines such as interleukin (IL) -6, IL-10 and tumor necrosis factor- α (TNF-α) have been reported. Many anti-viral drugs have been tried, but none were proven fully effective. Supportive care and management of the complications that are caused mainly by inflammation might be the key to greater survival rates and shorter hospitalization (e.g., the use of remdesivir, lopinavir, ritonavir, umifenovir (arbidol), oseltamivir, ganciclovir, favipiravir, darunavir, hydroxychloroquine, chloroquine, colchicine, azithromycin, anakinra, canakinumab, tocilizumab, siltuximab, sarilumab, Type 1 interferon, interferon β-1a, interferon α- 2b, baricitinib, ruxolitinib, fedratinib, methylprednisolone and dexamethasone). However, the efficacy of these treatments still needs well-planned clinical trials. In such trials, careful attention must be paid to the duration of the treatment, the onset of beneficial effects, and the severity of the disease, otherwise, the outcomes may still remain inconclusive. Herein, we present a review of the current drugs, which are being used in the management of the disease and their anti-inflammatory properties. We also investigated if these drugs directly interact with Angiotensin-Converting Enzyme (ACE 2), which is a crucial component of the virus entry to the cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32735768</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>10</Day></DateCompleted><DateRevised><Year>2020</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1482-1826</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><PubDate><Year>2020</Year></PubDate></JournalIssue><Title>Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques</Title><ISOAbbreviation>J Pharm Pharm Sci</ISOAbbreviation></Journal><ArticleTitle>Anti-Inflammatory Properties of Drugs Used to Control COVID-19 and their Effects on the Renin-Angiotensin System and Angiotensin-Converting Enzyme-2.</ArticleTitle><Pagination><MedlinePgn>259-277</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.18433/jpps31346</ELocationID><Abstract><AbstractText>COVID-19 infection is associated with systemic inflammation, and sometimes hyperinflammatory responses with cytokine storm. This plays a major role in COVID-19 severity and poor disease prognosis, even death. Higher levels of inflammatory hallmarks including C-reactive protein, ferritin, D-dimers, and cytokines such as interleukin (IL) -6, IL-10 and tumor necrosis factor- α (TNF-α) have been reported. Many anti-viral drugs have been tried, but none were proven fully effective. Supportive care and management of the complications that are caused mainly by inflammation might be the key to greater survival rates and shorter hospitalization (e.g., the use of remdesivir, lopinavir, ritonavir, umifenovir (arbidol), oseltamivir, ganciclovir, favipiravir, darunavir, hydroxychloroquine, chloroquine, colchicine, azithromycin, anakinra, canakinumab, tocilizumab, siltuximab, sarilumab, Type 1 interferon, interferon β-1a, interferon α- 2b, baricitinib, ruxolitinib, fedratinib, methylprednisolone and dexamethasone). However, the efficacy of these treatments still needs well-planned clinical trials. In such trials, careful attention must be paid to the duration of the treatment, the onset of beneficial effects, and the severity of the disease, otherwise, the outcomes may still remain inconclusive. Herein, we present a review of the current drugs, which are being used in the management of the disease and their anti-inflammatory properties. We also investigated if these drugs directly interact with Angiotensin-Converting Enzyme (ACE 2), which is a crucial component of the virus entry to the cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gilzad-Kohan</LastName><ForeName>Hamed</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Western New England University College of Pharmacy Department of Pharmaceutical and Administrative Sciences.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jamali</LastName><ForeName>Fakhreddin</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Canada</Country><MedlineTA>J Pharm Pharm Sci</MedlineTA><NlmUniqueID>9807281</NlmUniqueID><ISSNLinking>1482-1826</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.15.1</RegistryNumber><NameOfSubstance UI="D007703">Peptidyl-Dipeptidase A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.17.23</RegistryNumber><NameOfSubstance UI="C000705307">ACE2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.17.23</RegistryNumber><NameOfSubstance UI="D000085962">Angiotensin-Converting Enzyme 2</NameOfSubstance></Chemical></ChemicalList><SupplMeshList><SupplMeshName Type="Protocol" UI="C000705127">COVID-19 drug treatment</SupplMeshName></SupplMeshList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000085962" MajorTopicYN="N">Angiotensin-Converting Enzyme 2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="N">COVID-19</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012084" MajorTopicYN="N">Renin-Angiotensin System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>8</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>8</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32735768</ArticleId><ArticleId IdType="doi">10.18433/jpps31346</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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