RESUMO
Stroke is consistently one of the top ten causes of morbidity and mortality globally, whose outcomes are quite variable, necessitating case-specific management. Prophylactic diets before the onset of stroke have been implicated to work. In this research, the effects of virgin coconut oil (VCO) on stroke were evaluated using a stroke-prone spontaneously hypertensive rat (SHRSP) model. Eight-week-old SHRSPs were subjected to the repeated oral administration (5 mL/kg/day) of either 1% Tween 80 (group A) or VCO (group B). An early stroke onset was observed due to hypertension that was aggravation by the administration of 1% NaCl in water ad libitum. The following data were collected: the days until stroke occurred, the survival rate until the animal died, and blood pressure (BP) every two weeks using the tail-cuff method. After necropsy, the organs were harvested, and the brain was processed for a routine histopathological analysis. VCO delayed the incidence of it and prolonged their survival. Compared to group A, group B showed a significantly lowered BP by 20 mmHg at four weeks after the start of VCO treatment. Lastly, the brain histopathology showed that the structurally damaged areas were smaller in group B than they were in group A. The VCO could have protective effects on the brain before and even after stroke incidence.
RESUMO
Ticks are important vectors of diseases affecting both humans and animals. To be an efficient vector, ticks have to survive infection by pathogens such as the Langat virus (LGTV). One method utilized by ticks is their complex antioxidant mechanism. Included in the vast antioxidant processes are several enzymes involved in redox homeostasis. The ubiquitous glutathione S-transferases (GSTs) belong to the antioxidant family of enzymes. In this study, we evaluated the role of a GST during LGTV infection. ISE6 cells were infected with LGTV with a multiplicity of infection (MOI) of 0.01 and observed daily. The infection success was monitored via indirect immunofluorescent antibody test (IFAT) for LGTV for up to 4 days. The gene expression of IsGST1 was determined by real-time polymerase chain reaction (PCR) using IsGST1 gene-specific primers. Knockdown of the IsGST1 gene with subsequent LGTV infection was also performed. Afterward, ISE6 cell mortality and viability were checked daily until the fourth day. The virus titer from supernatants of IsGST1-knockdown cells was quantified using a focus-formation assay. IFAT data showed that LGTV infects ISE6 cells in a time-dependent manner with increasing infection from day 0 to day 4. The IsGST1 genes showed an increasing expression until day 2 of infection, while decreased expression was observed from day 3 to day 4 post-infection. Knockdown of the IsGST1 resulted in increased mortality on the third day of infection, while the cell viability was also negatively affected by the knockdown of the IsGST1 genes from day 0 to day 4 post-infection. Knockdown of the IsGST1 genes also resulted in a decreased viral titer from the supernatants of the ISE6 cells infected with LGTV. Based on the results, GSTs are possibly utilized both by cells and the virus for mutual survival and proliferation.
