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dc.contributor.authorReg.No:BO0119004-
dc.date.accessioned2023-03-30T14:14:32Z-
dc.date.available2023-03-30T14:14:32Z-
dc.date.issued2022-
dc.identifier.urihttp://localhost:8080/xmlui/handle/123456789/1374-
dc.description.abstractIntroduction: Depression or Depressive Disorder is a common mental disorder that presents with depressed mood, loss of interest or pleasure, decreased energy, feelings of guilt or low self-worth, disturbed sleep or appetite, and poor concentration. Recent advances in neurobiological research have shown a growing body of evidence indicating inflammatory pathways have a role in the genesis of depression. Depression is caused by a complex combination of behavioural, neurotropic, immunological, neuroendocrine, and other physiological components. Excessive secretion of proinflammatory cytokines, such as interleukin-1 beta (IL-1), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-), causes sickness behavior, which has symptoms that are similar to those of depression, implying that cytokines have a role in depression. However, the current therapy available is with limited efficacy serious side effects. Objective of the study: 1. To study the effect of Ranolazine and Trimetazidine on Depression paradigm. 2. To compare Ranolazine and Trimetazidine with that of standard anti-depressant drug Fluoxetineen_US
dc.language.isoen_USen_US
dc.publisherKLE Academy of Higher Education and Research, Belagavien_US
dc.subjectRanolazine, Depression, Coronary Artery Disease, Forced Swim Test, Inflammation, CUMS, FST, TST.en_US
dc.titleEffect of Ranolazine and Trimetazidine on Depression Paradigm in Male Swiss Albino Miceen_US
dc.typeDissertationsen_US
Appears in Collections:Pharmacology

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