Anti-diabetic potential of the essential oil of Pinus koraiensis leaves toward streptozotocin-treated mice and HIT-T15 pancreatic β cells

Cited 17 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorH E Joo-
dc.contributor.authorHyo Jung Lee-
dc.contributor.authorE J Sohn-
dc.contributor.authorM H Lee-
dc.contributor.authorH S Ko-
dc.contributor.authorS J Jeong-
dc.contributor.authorH J Lee-
dc.contributor.authorS H Kim-
dc.date.accessioned2017-04-19T09:46:47Z-
dc.date.available2017-04-19T09:46:47Z-
dc.date.issued2013-
dc.identifier.issn0916-8451-
dc.identifier.uri10.1271/bbb.130254ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11671-
dc.description.abstractThe metabolic syndrome creates risk factors for coronary heart disease, diabetes, fatty liver, obesity and several cancers. Our group has already reported that the essential oil from leaves of Pinus koraiensis SIEB (EOPK) exerted antihyperlipidemic effects by upregulating the low-density lipoprotein receptor and inhibiting acyl-coenzyme A, cholesterol acyltransferases. We evaluated in the current study the anti-diabetic effects of EOPK on mice with streptozotocin (STZ)-induced type I diabetes and on HIT-T15 pancreatic β cells. EOPK significantly protected HIT-T15 cells from STZ-induced cytotoxicity and reduced the blood glucose level in STZinduced diabetic mice when compared with the untreated control. EOPK consistently and significantly suppressed the α-amylase activity in a dose-dependent manner and enhanced the expression of insulin at the mRNA level in STZ-treated HIT-T15 cells, while the expression of insulin was attenuated. EOPK also significantly abrogated the population of reactive oxygen species when compared to the untreated control in STZ-treated HIT-T15 cells. Furthermore, EOPK significantly reduce nitric oxide production, suppressed the phosphorylation of endothelial nitric oxide (NO) synthase and suppressed the production of vascular endothelial growth factor (VEGF) in STZ-treated HIT-T15 cells, implying its potential application to diabetic retinopathy. Overall, our findings suggest that EOPK had hypoglycemic potential by inhibiting reactive oxygene species (ROS), endothelial NO synthase (eNOS) and VEGF in STZ-treated mice and HIT-T15 pancreatic β cells as a potent anti-diabetic agent.-
dc.publisherT&F (Taylor & Francis)-
dc.titleAnti-diabetic potential of the essential oil of Pinus koraiensis leaves toward streptozotocin-treated mice and HIT-T15 pancreatic β cells-
dc.title.alternativeAnti-diabetic potential of the essential oil of Pinus koraiensis leaves toward streptozotocin-treated mice and HIT-T15 pancreatic β cells-
dc.typeArticle-
dc.citation.titleBioscience Biotechnology and Biochemistry-
dc.citation.number10-
dc.citation.endPage2001-
dc.citation.startPage1997-
dc.citation.volume77-
dc.contributor.affiliatedAuthorHyo Jung Lee-
dc.contributor.alternativeName주혜은-
dc.contributor.alternativeName이효정-
dc.contributor.alternativeName손은정-
dc.contributor.alternativeName이민호-
dc.contributor.alternativeName고현숙-
dc.contributor.alternativeName정수진-
dc.contributor.alternativeName이효정-
dc.contributor.alternativeName김성훈-
dc.identifier.bibliographicCitationBioscience Biotechnology and Biochemistry, vol. 77, no. 10, pp. 1997-2001-
dc.identifier.doi10.1271/bbb.130254-
dc.subject.keywordHIT-T15 cell-
dc.subject.keywordPinus koraiensis-
dc.subject.keywordStreptozotocin-
dc.subject.keywordVascular endothelial growth factor (VEGF)-
dc.subject.localHIT-T15 cell-
dc.subject.localPinus koraiensis-
dc.subject.localstreptozotocin-
dc.subject.localstreptozotocin (STZ)-
dc.subject.localStreptozotocin-
dc.subject.localvascular endothelial growth factor-
dc.subject.localVascular endothelial growth factor (VEGF)-
dc.subject.localvascular endothelial growth factor (VEGF)-
dc.subject.localVascular endothelial growth factor-
dc.description.journalClassY-
Appears in Collections:
1. Journal Articles > Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.