ABSTRACT
The impact of Rg1 in the disease progress and pathology of amyotrophic lateral sclerosis (ALS) was investigated in mouse model (SOD1 G93A). Body weight and survival rate were monitored to check the course of disease. Rotarod test was used to evaluate the coordination of muscle movement. Toluidine blue staining and immunofluorescence were used to check the effect of Rg1 on motor neuron and microglia. The expression of oxidative stress related protein Nrf2 and the miRNA were tested to investigate the mechanism of Rg1. We found that 20 mg·kg-1·d-1 Rg1 significantly postponed the disease onset and process, improved the motor syndrome, reduced the loss of motor neuron and inhibited the activation of microglia cells. Rg1 inhibited the aggregation of miR-153 in the spinal cord of ALS mice, which relieved the inhibition of Nrf2 and contributed to its up-regulation in the activation of HO-1 anti-oxidative signal pathway. Our study confirmed that Rg1 could protect ALS mice from oxidative damage through the up-regulation of miR-153/Nrf2/HO-1, which provides a theoretical foundation for Rg1 application to the ALS treatment.
ABSTRACT
This study was designed to test the effect of short-term high-fat diet feeding on the cognitive impairment in a rat model of Alzheimer's disease. After establishment of Alzheimer's disease model, the rats were fed on a high-fat diet, and subjected to water maze (Morris water maze, MWM) behavioral test for learning and memory ability. Western blot was used to detect the expression of caspase-1 pathway. The results showed that short-term high-fat diet could alleviate the damage of okada acid in Morris water maze. The mechanism may be mediated by the regulation of the NLRP3/caspase-1 signaling pathway, which alleviates neuronal damage, resulting in a protective effect.