Lactuside B decreases aquaporin-4 and caspase-3 mRNA expression in the hippocampus and striatum following cerebral ischaemia-reperfusion injury in rats

Abstract

This study aimed to investigate the effects of lactuside B (LB) on aquaporin-4 (AQP4) and caspase-3 mRNA expression in the hippocampus and the striatum following cerebral ischaemia-reperfusion (I/R) injury in rats. Cerebral I/R injury was established in Sprague-Dawley rats by occluding the middle cerebral artery for 2 h and then inducing reperfusion. Rats in the I/R + LB groups were treated with various doses of LB following reperfusion. Neurological deficit scores and brain water content were obtained to determine the pharmacodynamics of LB. Reverse transcription polymerase chain reaction was performed to determine the expression levels of AQP4 and caspase-3 mRNA in the hippocampus and the striatum. The results of the present study indicate that LB decreased the neurological deficit scores and the brain water content. In the hippocampus, AQP4 and caspase-3 mRNA expression levels were significantly downregulated in the I/R + LB groups at 24 and 72 h following drug administration, compared with those in the I/R group (P<0.05). In the striatum, LB was also shown to significantly reduce AQP4 and caspase-3 mRNA expression levels at 24 and 72 h following drug administration, compared with those in the I/R group (P<0.05). The effects became stronger as the LB dose was increased. The most significant reductions in AQP4 and caspase-3 mRNA expression were noted in the I/R + LB 25 mg/kg and I/R + LB 50 mg/kg groups at 72 h following drug administration. The results of the present study show that LB is capable of significantly downregulating AQP4 and caspase-3 mRNA expression in the hippocampus and striatum following cerebral I/R injury in rats. The mechanism by which LB improved ischaemic brain injury may be associated with changes in AQP4 and caspase-3 mRNA expression in the hippocampus and the striatum.

Physical exercise prevents motor disorders and striatal oxidative imbalance after cerebral ischemia-reperfusion

“…Animals subjected to ischemia-reperfusion also experienced oxidative stress resulting in oxidative imbalance in the striatum. The damage observed in the striatum is consistent with the neuromotor deficits observed in the ischemia-reperfusion group ( 9 ). In this study, neuromotor impairment was demonstrated by the results of the rotarod and open-field tests.…”

“…Under conditions of oxidative stress, cells are unable to balance the deleterious effects of ROS through antioxidant mechanisms ( 8 ). Some brain regions, including the striatum, appear to be particularly susceptible to oxidative damage due to ROS levels ( 9 ). The striatum plays an important role in the control of voluntary movements ( 10 ) and contains a high concentration of dopaminergic receptors, which are responsible for motor activation ( 11 ).…”