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Abstract
AL-1 is a novel andrographolide derivative synthesized by conjugating andrographolide and alpha lipoic acid. AL-1 has been found to increase insulin secretion, decrease blood glucose level and protect β-cell mass and function in alloxan-induced diabetic mouse model. However, the protective mechanism of AL-1 on high glucose-induced pancreatic β-cell injury is still not clear. In the present study, we found that AL-1 reduced reactive oxygen species (ROS) and nitric oxide (NO) generation induced by high glucose in RIN-m cells, and which elevated the activities of superoxide dismutase (SOD) and catalase (CAT). In addition, AL-1 increased the expression of NF-E2-related factor 2 (Nrf2), thioredoxin-1 (Trx-1) and heme oxygenase-1 (HO- 1) proteins in RIN-m cells. These results suggest that AL-1 prevented RIN-m cells from high glucose-induced oxidative damage via upregulation of Nrf2 signaling pathway.
Keywords: Andrographolide, α-Lipoic acid, Nrf2, ROS.
Current Pharmaceutical Design
Title:Protective effects of andrographolide derivative AL-1 on high glucose-induced oxidative stress in RIN-m cells
Volume: 22 Issue: 4
Author(s): Hui Yan, Yongmei Li, Yali Yang, Zaijun Zhang, Gaoxiao Zhang, Yewei Sun, Pei Yu, Yuqiang Wang and Lipeng Xu
Affiliation:
Keywords: Andrographolide, α-Lipoic acid, Nrf2, ROS.
Abstract: AL-1 is a novel andrographolide derivative synthesized by conjugating andrographolide and alpha lipoic acid. AL-1 has been found to increase insulin secretion, decrease blood glucose level and protect β-cell mass and function in alloxan-induced diabetic mouse model. However, the protective mechanism of AL-1 on high glucose-induced pancreatic β-cell injury is still not clear. In the present study, we found that AL-1 reduced reactive oxygen species (ROS) and nitric oxide (NO) generation induced by high glucose in RIN-m cells, and which elevated the activities of superoxide dismutase (SOD) and catalase (CAT). In addition, AL-1 increased the expression of NF-E2-related factor 2 (Nrf2), thioredoxin-1 (Trx-1) and heme oxygenase-1 (HO- 1) proteins in RIN-m cells. These results suggest that AL-1 prevented RIN-m cells from high glucose-induced oxidative damage via upregulation of Nrf2 signaling pathway.
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Cite this article as:
Yan Hui, Li Yongmei, Yang Yali, Zhang Zaijun, Zhang Gaoxiao, Sun Yewei, Yu Pei, Wang Yuqiang and Xu Lipeng, Protective effects of andrographolide derivative AL-1 on high glucose-induced oxidative stress in RIN-m cells, Current Pharmaceutical Design 2016; 22 (4) . https://dx.doi.org/10.2174/1381612821666150921110716
DOI https://dx.doi.org/10.2174/1381612821666150921110716 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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