Abstract
BackgroundThis study was carried out to investigate the effect of total flavonoids of Spatholobus suberectus Dunn (TFSD) on PCV2 induced oxidative stress in RAW264.7 cells.MethodsOxidative stress model was established in RAW264.7 cells by infecting with PCV2. Virus infected cells were then treated with various concentrations (25 mg/ml, 50 mg/ml and 100 mg/ml) of TFSD. The levels of oxidative stress related molecules (NO, ROS, GSH and GSSG) and activities of associated enzymes (SOD, MPO and XOD were analyzed using ultraviolet spectrophotometry, fluorescence method and commercialized detection kits.ResultsPCV2 infection induced significant increase of NO secretion, ROS generation, GSSG content, activities of both XOD and MPO, and dramatically decrease of GSH content and SOD activity in RAW264.7 cells (P < 0.05). After treating with TFSD, PCV2 induced alteration of oxidative stress related molecule levels and enzyme activities were recovered to a level similar to control.ConclusionOur findings indicated that TFSD was able to regulate oxidative stress induced by PCV2 infection in RAW264.7 cells, which supports the ethnomedicinal use of this herb as an alternative or complementary therapeutic drug for reactive oxygen-associated pathologies.
Highlights
This study was carried out to investigate the effect of total flavonoids of Spatholobus suberectus Dunn (TFSD) on Porcine circovirus type 2 (PCV2) induced oxidative stress in RAW264.7 cells
When the concentration of TFSD was lower than 100 μg/mL, the cell viability were greater than 80% and no significant difference has been observed when compared to control
Vitamin C, a widely used antioxidant, was able to inhibit the elevation of nitric oxide (NO) and reactive oxygen species (ROS) content induced by PCV2 infection
Summary
This study was carried out to investigate the effect of total flavonoids of Spatholobus suberectus Dunn (TFSD) on PCV2 induced oxidative stress in RAW264.7 cells. PCV2 infection induces oxidative stress and immunosuppression in pigs which further facilitate virus replication [14]. It has been reported that there was a time-dependent increase in ROS following PCV2 infection and oxidative stress induced by H2O2 enhanced PCV2 replication in PK-15 cells. Antioxidant N-acetyl-l-cysteine (NAC) treatment was able to inhibited PCV2 replication inside the kidney cells, whereas GSH depletion with buthionine sulfoximine (BSO) resulted in elevation of ROS levels and increased PCV2 replication [15]. PCV2 infection might be promoted by ROS-induced NF-κB activation, as inhibiting the activity of NF-κB, a redox-responsive transcription factor, suppressed BSO-mediated increase of PCV2 replication [15]. PCV2 infection induced elevation of ROS level and release of proinflammatory factors, such as IL-1β, IL-10, IL-8 and TNF-α, resulting in decrease of
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