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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록· 키워드
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Objectives: This study examined whether Lycii Radicis Cortex has an inhibitory effect on inflammatory response through an oxidative stress and advanced glycation endproducts (AGEs)-mediated pathway in streptozotocin (STZ)-induced type 1 diabetic rats.
Methods: Lycii Radicis Cortex was orally administered to STZ-induced diabetic rats in doses of 80 or 160 mg/kg body weight/day for 2 weeks, and its effects were compared with those of diabetic control and normal rats.
Results: The administration of Lycii Radicis Cortex decreased the elevated serum urea nitrogen and renal reactive oxygen species (ROS), and reduced the increased AGEs in the serum and kidney. The elevated protein expressions of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits in the kidney of diabetic control rats were significantly decreased after Lycii Radicis Cortex treatments. Moreover, the kidney of diabetic rats exhibited the up-regulation of receptor for AGEs (RAGE) and AGEs-related proteins; however, Lycii Radicis Cortex treatment also significantly reduced those expressions (excepted RAGE). In addition, the diabetic rats exhibited an up-regulation of the expression of proteins related to inflammation in the kidney, but Lycii Radicis Cortex administration reduced significantly the expression of the inflammatory proteins through the nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1) pathways.
Conclusions: This study provides scientific evidence that Lycii Radicis Cortex exerts the antidiabetic effect by inhibiting the expressions of AGEs and NF-κB in the STZ-induced diabetic rats.
Methods: Lycii Radicis Cortex was orally administered to STZ-induced diabetic rats in doses of 80 or 160 mg/kg body weight/day for 2 weeks, and its effects were compared with those of diabetic control and normal rats.
Results: The administration of Lycii Radicis Cortex decreased the elevated serum urea nitrogen and renal reactive oxygen species (ROS), and reduced the increased AGEs in the serum and kidney. The elevated protein expressions of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits in the kidney of diabetic control rats were significantly decreased after Lycii Radicis Cortex treatments. Moreover, the kidney of diabetic rats exhibited the up-regulation of receptor for AGEs (RAGE) and AGEs-related proteins; however, Lycii Radicis Cortex treatment also significantly reduced those expressions (excepted RAGE). In addition, the diabetic rats exhibited an up-regulation of the expression of proteins related to inflammation in the kidney, but Lycii Radicis Cortex administration reduced significantly the expression of the inflammatory proteins through the nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1) pathways.
Conclusions: This study provides scientific evidence that Lycii Radicis Cortex exerts the antidiabetic effect by inhibiting the expressions of AGEs and NF-κB in the STZ-induced diabetic rats.
목차
Introduction
Materials and Methods
Results
Discussion
Discussion
References
참고문헌 (46)
참고문헌 신청
[학술지(정기간행물)] - Peppa M / 2005 / Advanced glycation endproducts and diabetic complications : A general overview / Hormones 4 : 28 ~ 37
[학술지(정기간행물)] - Kikkawa R / 2013 / Progression of diabetic nephropathy / Am. J. Kidney Dis 41 : 19 ~ 21
[학술지(정기간행물)] - Forbes JM / 2008 / Oxidative stress as a major culprit in kidney disease in diabetes / Diabetes 57 : 1446 ~ 1454
[학술지(정기간행물)] - Ruderman N / 1992 / Glucose and diabetic vascular disease / FASEB J 6 : 2905 ~ 2914
[학술지(정기간행물)] - Schmidt AM / 1995 / The dark side of glucose / Nature (Med1) : 1002 ~ 1004
[학술지(정기간행물)] - Kikkawa R / 2013 / Progression of diabetic nephropathy / Am. J. Kidney Dis 41 : 19 ~ 21
[학술지(정기간행물)] - Forbes JM / 2008 / Oxidative stress as a major culprit in kidney disease in diabetes / Diabetes 57 : 1446 ~ 1454
[학술지(정기간행물)] - Ruderman N / 1992 / Glucose and diabetic vascular disease / FASEB J 6 : 2905 ~ 2914
[학술지(정기간행물)] - Schmidt AM / 1995 / The dark side of glucose / Nature (Med1) : 1002 ~ 1004
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UCI(KEPA) : I410-ECN-0101-2017-519-001005826