Conclusion
In chronic omethoate poisoning rats, NRG1β can promote the phosphorylation level of ERK1/2 in hippocampal neurons, and play an important role in the improvement of cognitive function.
Methods
Rats with strong learning and memory ability, 50 in total, were selected by Y-electric maze test. Among which, 15 rats were randomly selected into control group, and the rest 35 rats were used to establish experimental cognitive impairment models by being injected with omethoate subcutaneously. The 30 cases of successful cognitive impairment models were randomly divided into model group and treated group consisting of 15 rats, respectively. Then rats in treated group were injected with NRG1β into their lateral ventricles, while rats in control and model groups were given equal volume of PBS simultaneously. The cognitive capacity of rats was evaluated with Y-electric maze. The morphology and ultrastructure of hippocampus were observed by hematoxylin eosin (HE) staining and transmission electron microscopy (TEM) respectively. The expression of p-ERK1/2 was determined by immunohistochemical (IHC) staining and Western blotting.
Objective
To observe the effects of neuregulin1β (NRG1β) on the level of phosphorylated ERK1/2 (p-ERK1/2), and explore the therapeutic mechanism of NRG1β on the cognitive dysfunction in rats with chronic omethoate poisoning.
Results
Compared with rats in model group, the cognitive ability of rats with omethoate exposed (model and treated groups) reduced significantly, along with the obvious damage of hippocampal neurons and the expression of p-ERK1/2 decreased significantly (P < 0.05). And after treatment with NRG1β, the cognitive activity of treated rats was improved obviously, and the injury of hippocampal neurons was milder and the expression of p-ERK1/2 increased significantly more than those in model rats (P < 0.05).