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dc.contributor.authorGhaffari-Nasab, A
dc.contributor.authorMirzaie Bavil, F
dc.contributor.authorGhiasi, R
dc.contributor.authorSadigh-Eteghad, S
dc.contributor.authorAlipour, MR
dc.date.accessioned2018-08-26T04:53:31Z
dc.date.available2018-08-26T04:53:31Z
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/37936
dc.description.abstractDiabetes is associated with vascular complications and impaired angiogenesis. Since angiogenesis plays a crucial role in vascular homeostasis in ischemic heart diseases, in this study, the effect of IMOD™ on miR-503 and CDC25 expression level which are altered in impaired angiogenesis were investigated in heart tissue of diabetic rats.Forty male Wistar rats (200-250 g) were randomly classified into 4 groups: control (C), IMOD™ (I), diabetes (D), and diabetes+IMOD™ (D+I). For induction of experimental diabetes in animals, a single dose of streptozotocin (STZ; 60mg/kg) was injected intraperitoneally. After 8 weeks of treatment with IMOD™ (20 mg/kg/day), heart tissue samples were removed and used for measurement of miR-503 and CDC25 expression level as well as histological studies.Results of this study showed that diabetes decreased heart tissue angiogenesis which was associated with increased miR-503 and reduced CDC25 expression levels (p<0.05) and IMOD™ could reduce the expression of miR-503 and increase the expression of CDC25 (p<0.05). Moreover, IMOD™ extensively induced angiogenesis in the heart tissue of diabetic group. However, IMOD™ had no significant effect on expressions of miR-503 and CDC25, or angiogenesis in healthy rats.This study showed that IMOD™ is able to increase angiogenesis in the heart tissue of diabetic rats. The angiogenic effect of IMOD™ is associated with reduction of miR-503 expression and increased expression of CDC25.
dc.language.isoEnglish
dc.relation.ispartofAvicenna journal of phytomedicine
dc.titleEffects of IMOD™ on angiogenesis, miR-503 and CDC25 expression levels in heart tissue of diabetic male rats.
dc.typearticle
dc.citation.volume8
dc.citation.issue2
dc.citation.spage152
dc.citation.epage160
dc.citation.indexPubmed


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