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KMID : 1134820160450070929
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Journal of the Korean Society of Food Science and Nutrition
2016 Volume.45 No. 7 p.929 ~ p.937
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Beneficial Effects of Acanthopanax senticosus Extract in Type Ⅱ Diabetes Animal Model via Down-Regulation of Advanced Glycated Hemoglobin and Glycosylation End Products
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Kwon Han-Al
Lee Min-Hee
Kim Yong-Jae
Kim Eun
Kim Ok-Kyung
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Abstract
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The purpose of this study was to investigate the effect of Acanthopanax senticosus extract (ASE) (ethanol:DW=1:1, v/v) on inhibition of type 2 diabetes using an OLETF rat model via regulation of HbA1c and AGEs levels. Supplementation with ASE 0.1% and 0.5% effectively lowered levels of glucose, insulin, oral glucose tolerance test, and Homa-insulin resistance, suggesting reduced insulin resistance. Blood levels of HbA1c and AGEs were significantly reduced in a dose-dependent manner. As oxidative stress plays a key role in accelerating production of HbA1c and AGEs, which worsen symptoms of type 2 diabetes, levels of malonaldehyde and pro-inflammatory cytokines were measured. Lipid peroxidation in both blood and liver tissues was significantly reduced, and induction of pro-inflammatory cytokines interleukin-β and tumor necrosis factor-α, which elevate production of HbA1c and AGEs, was inhibited (P<0.05). To evaluate the possible cellular events after AGEs receptor activation, genetic expression of protein kinase C (PKC)-δ and transforming growth factor (TGF)-β was measured by real-time polymerase chain reaction. Supplementation with both ASE 0.1% and 0.5% significantly inhibited mRNA expression of PKC-δ and TGF-β, indicating that ASE may have beneficial effects on preventing insulin-resistant cells or tissues from progressing to diabetic complications. Taken together, ASE has potential to improve type 2 diabetes by inhibiting insulin resistance and protein glycosylation, including production of HbA1c and AGEs. Anti-oxidative activities of ASE are a main requisite for reducing production of HbA1c and AGEs and are also related to regulation of the PKC signaling pathway, resulting in suppression of TGF-β, which increases synthesis of collagen, prostaglandin, and disease-related proteins.
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KEYWORD
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Acanthopanax senticosus, type Ⅱ diabetes, glycosylation end products, HbA1c, oxidative stress
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