The Antioxidant Effects of Cardamonin in LPS‐Activated BV‐2 Microglial Cells

Abstract

Chronic oxidative stress and inflammation are implicated in the development and progression of several neurodegenerative diseases. The continuous over-activation of the microglia cells produces numerous factors, including nitric oxide and reactive oxygen species, which induce neurodegeneration. Many natural compounds with anti-inflammatory and antioxidative effects can protect neurons from oxidative stress. Cardamonin is an important bioactive compound found in many plants, such as Alpinia katsumadai and Alpinia conchigera. It has been reported to have multiple therapeutic properties, which include anti-cancer, anti-inflammatory, antioxidant, antiviral antibiotic, antifungal, and antiallergic activities. The present study examined the effects of cardamonin on LPS-activated BV-2 microglial cells. In this study, cell viability results showed increasing concentrations of cardamonin, ranging from 0.78 to 200 uM induced BV-2 cells cytotoxicity in a dose-response manner. The selected concentration used for further studies was 6.25 uM based on a rate of at least 80% of cells alive. In the nitric oxide assay, cardamonin concentrations of 6.25uM significantly reduced nitric oxide release in LPS-activated BV-2 cells, compared to the cells treated with LPS only (p < 0.001). Although cardamonin was not effective in reducing the formation of H2O2 of the LPS-activated cells, it significantly decreased the cellular production of SOD 3-fold (p < 0.05). It also, increased the levels of expression of CAT 2.5-fold (p < 0.05) and glutathione 2-fold (p < 0.05) in the LPS activated BV-2 cells. The effect of cardamonin on the activity of antioxidant enzymes in BV-2 microglial cells reflects a decreased oxidative stress status in the cellular environment. These findings suggest that cardamonin may be utilized in the therapy of neurodegeneration caused by excessive oxidative stress. Cardamonin use may also help delay the onset of neurodegenerative diseases or prevent their progression in the CNS.