- P-ISSN 1010-0695
- E-ISSN 2288-3339
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- P-ISSN1010-0695
- E-ISSN2288-3339
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The Effects of Lycii Radicis Cortex on Inflammatory Response through an Oxidative Stress and AGEs-mediated Pathway in STZ-induced Diabetic Rats
Journal of Korean Medicine / Journal of Korean Medicine, (P)1010-0695; (E)2288-3339
2016, v.37 no.2, pp.62-75
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(2016). The Effects of Lycii Radicis Cortex on Inflammatory Response through an Oxidative Stress and AGEs-mediated Pathway in STZ-induced Diabetic Rats. Journal of Korean Medicine, 37(2), 62-75.
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Abstract
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.
- keywords
- Lycii Radicis Cortex, Type 1 Diabetes, Oxidative Stress, Nuclear Factor-kappa B, Advanced Glycation Endproduct.
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