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.
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