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Classical swine fever virus induces oxidative stress in swine umbilical vein endothelial cells.

He L, Zhang Y, Fang Y, Liang W, Lin J, Cheng M - BMC Vet. Res. (2014)

Bottom Line: In addition, antioxidants showed significant inhibitory effects on the CSFV replication, indicating a close relationship between CSFV replication and OS induced in the host cells.Our results indicated that CSFV infection induced oxidative stress in SUVECs.These findings provide novel information on the mechanism by which CSFV can alter intracellular events associated with the viral infection.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine, Northwest A & F University, Yangling, Shaanxi, 712100, P.R. China. helei4280546@163.com.

ABSTRACT

Background: Classical swine fever virus (CSFV) infection causes significant losses of pigs, which is characterized by hemorrhage, disseminated intravascular coagulation and leucopenia. The swine vascular endothelial cell is a primary target cell for CSFV. The aim of this study was to determine the role of CSFV infection in inducing oxidative stress (OS) in vascular endothelial cells.

Results: We demonstrated that CSFV infection induced oxidative stress in swine umbilical vein endothelial cells (SUVECs), characterized by the induction of reactive oxygen species (ROS) production and the elevations of porcine antioxidant proteins thioredoxin (Trx), peroxiredoxin-6 (PRDX-6) and heme oxygenase-1 (HO-1) expression. Furthermore, cyclooxygenase-2 (COX-2), a pro-inflammatory protein related to oxidative stress, was up-regulated while anti-inflammatory protein peroxisome proliferator-activated receptor-γ (PPAR-γ), an important mediator in vascular functional regulation, was down-regulated in the CSFV infected cells. In addition, antioxidants showed significant inhibitory effects on the CSFV replication, indicating a close relationship between CSFV replication and OS induced in the host cells.

Conclusions: Our results indicated that CSFV infection induced oxidative stress in SUVECs. These findings provide novel information on the mechanism by which CSFV can alter intracellular events associated with the viral infection.

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Inhibition of CSFV RNA replication by antioxidants in cultured SUVEC cells. The amount of viral genome was measured by real-time RT-PCR, which was normalized to the corresponding β-actin in the same sample. The mean of three repeat experiments performed in triplicate is shown, and error bars represent the SD.
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Fig7: Inhibition of CSFV RNA replication by antioxidants in cultured SUVEC cells. The amount of viral genome was measured by real-time RT-PCR, which was normalized to the corresponding β-actin in the same sample. The mean of three repeat experiments performed in triplicate is shown, and error bars represent the SD.

Mentions: To determine whether the oxidative stress induced by CSFV infection is involved in the viral replication or not, oxidative stress inhibitors glutathione (GSH), N-acetyl-L-cysteine (NAC), butylated hydroxyanisole (BHA) and curcumin, which were reported to counteract the oxygen free radical, were added to the CSFV infected cells. Quantitative real-time RT-PCR was carried out by using the lysates prepared from SUVECs, SUVECs infected with CSFV and CSFV infected cells incubated with GSH, NAC, BHA and curcumin and the COX-2 inhibitor aspirin (ASA) for 72 h, respectively. Results showed that the amount of viral RNA was significantly reduced in the presence of antioxidants in varying degrees (Figure 7), indicating a close association between oxidative stress induced by CSFV and viral replication.Figure 7


Classical swine fever virus induces oxidative stress in swine umbilical vein endothelial cells.

He L, Zhang Y, Fang Y, Liang W, Lin J, Cheng M - BMC Vet. Res. (2014)

Inhibition of CSFV RNA replication by antioxidants in cultured SUVEC cells. The amount of viral genome was measured by real-time RT-PCR, which was normalized to the corresponding β-actin in the same sample. The mean of three repeat experiments performed in triplicate is shown, and error bars represent the SD.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4270048&req=5

Fig7: Inhibition of CSFV RNA replication by antioxidants in cultured SUVEC cells. The amount of viral genome was measured by real-time RT-PCR, which was normalized to the corresponding β-actin in the same sample. The mean of three repeat experiments performed in triplicate is shown, and error bars represent the SD.
Mentions: To determine whether the oxidative stress induced by CSFV infection is involved in the viral replication or not, oxidative stress inhibitors glutathione (GSH), N-acetyl-L-cysteine (NAC), butylated hydroxyanisole (BHA) and curcumin, which were reported to counteract the oxygen free radical, were added to the CSFV infected cells. Quantitative real-time RT-PCR was carried out by using the lysates prepared from SUVECs, SUVECs infected with CSFV and CSFV infected cells incubated with GSH, NAC, BHA and curcumin and the COX-2 inhibitor aspirin (ASA) for 72 h, respectively. Results showed that the amount of viral RNA was significantly reduced in the presence of antioxidants in varying degrees (Figure 7), indicating a close association between oxidative stress induced by CSFV and viral replication.Figure 7

Bottom Line: In addition, antioxidants showed significant inhibitory effects on the CSFV replication, indicating a close relationship between CSFV replication and OS induced in the host cells.Our results indicated that CSFV infection induced oxidative stress in SUVECs.These findings provide novel information on the mechanism by which CSFV can alter intracellular events associated with the viral infection.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine, Northwest A & F University, Yangling, Shaanxi, 712100, P.R. China. helei4280546@163.com.

ABSTRACT

Background: Classical swine fever virus (CSFV) infection causes significant losses of pigs, which is characterized by hemorrhage, disseminated intravascular coagulation and leucopenia. The swine vascular endothelial cell is a primary target cell for CSFV. The aim of this study was to determine the role of CSFV infection in inducing oxidative stress (OS) in vascular endothelial cells.

Results: We demonstrated that CSFV infection induced oxidative stress in swine umbilical vein endothelial cells (SUVECs), characterized by the induction of reactive oxygen species (ROS) production and the elevations of porcine antioxidant proteins thioredoxin (Trx), peroxiredoxin-6 (PRDX-6) and heme oxygenase-1 (HO-1) expression. Furthermore, cyclooxygenase-2 (COX-2), a pro-inflammatory protein related to oxidative stress, was up-regulated while anti-inflammatory protein peroxisome proliferator-activated receptor-γ (PPAR-γ), an important mediator in vascular functional regulation, was down-regulated in the CSFV infected cells. In addition, antioxidants showed significant inhibitory effects on the CSFV replication, indicating a close relationship between CSFV replication and OS induced in the host cells.

Conclusions: Our results indicated that CSFV infection induced oxidative stress in SUVECs. These findings provide novel information on the mechanism by which CSFV can alter intracellular events associated with the viral infection.

Show MeSH
Related in: MedlinePlus