Evaluation of Changes in Biomarkers of Oxidative Stress Response in the Brain of Mice Infected with Street Rabies Virus

The rabies virus infection leads to 60,000 deaths worldwide each year and is considered an economic and social hazard. Although our knowledge of the rabies virus replication and its interaction with the host cell is in its infancy, it helps us design optimal drugs and vaccines. Therefore, the aim of this study was to evaluate the changes in catalase and superoxide dismutase (SOD) enzymes, nitric oxide (NO) chemical composition and NF-κB gene activity as biomarkers of oxidative stress response in brain tissue of mice infected with street rabies virus.

In this experimental study, 16 21-day-old outbred mice were divided into two groups of healthy and experimental (n=8). After determining the titer of rabies virus, the mice in the experimental group received 0.03 ml of rabies virus with LD50 intracerebrally (IC) using Hamilton 0.25 ml syringe. To evaluate the changes of catalase, NO, and SOD enzymes, test kit and colorimetric method were used and NF-kB activity was evaluated by Real-Time PCR according to Sdha gene.

In this study, catalase activity in the brains of infected mice (0.14±0.007) was significantly reduced compared to healthy mice (control) (0.67±0.008) (p=0.01). In this experimental study, the SOD activity in the brains of infected mice (3±0.2 nmol/min/ml) was significantly reduced compared to healthy mice (control) (5.7 nmol/min/ml) (p=0.035). Evaluation of NO accumulation in the brain tissue of the infected group (9.0±0.04 mU/mg) was significantly increased compared to the healthy group (9.04±0.03 mU/mg) (p=0.025). Furthermore, the expression level of NF-κB in the brain of the mice infected with rabies virus was one tenth of the expression of this gene in the brain of healthy mice.

The results showed that rabies virus decreased the activity of catalase and SOD enzymes and increased nitric oxide. Furthermore, NF-κB expression decreased in the brain of mice infected with rabies virus, which may be due to the effect of the virus on the cellular signaling pathway.