AI Article Synopsis
- The study investigates how magnesium lithospermate B (LAB) affects the production of reactive oxygen species (ROS) in HEK293T cells exposed to high glucose levels or hydrogen peroxide (H2O2).
- It finds that LAB significantly reduces ROS levels and enhances the expression of heme oxygenase-1 (HO-1) in a way that depends on both the glucose concentration and the LAB dose.
- The results suggest that the protective effects of LAB against oxidative damage are mediated by the Nrf2 signaling pathway, highlighting its potential role in cellular defense mechanisms.
Article Abstract
Objectives: To investigate the effects of magnesium lithospermate B (LAB) on intracellular reactive oxygen species (ROS) production induced by high dose of glucose or H(2)O(2), we explored the influences of LAB on the expression of heme oxygenase-1 (HO-1) and nuclear factor E2-related factor-2 (Nrf2) in HEK293T cells after treatment with high dose of glucose.
Materials And Methods: The total nuclear proteins in HEK293T cells were extracted with Cytoplasmic Protein Extraction Kit. The ROS level was determined by flow cytometry. The mRNA and protein expression of HO-1 and Nrf2 were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot.
Results: LAB reduced the ROS production in HEK293T cells cultured under oxidative stress. High dose of glucose enhanced the expression of HO-1 mRNA and HO-1 protein in a time-dependent manner. LAB enhanced the expression of HO-1 mRNA and HO-1 protein in a dose-dependent manner treated with high dose of glucose. The amount of Nrf2 translocation was enhanced after cells were pretreated with 50μmol/L or 100μmol/L LAB. Silencing of Nrf2 gene eliminated the enhanced expression of HO-1 protein induced by high dose of glucose plus LAB.
Conclusions: LAB plays an important role against glucose-induced intracellular oxidative damage. The enhanced expression of HO-1 mRNA and HO-1 protein caused by LAB is regulated via Nrf2 signal pathway.
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| http://dx.doi.org/10.1016/j.bbrc.2011.06.071 | DOI Listing |
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