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N-Butylphthalide Improves Cognitive Function in Rats after Carbon Monoxide Poisoning
Ming-Jun Bi1, Xian-Ni Sun2, Yong Zou3
1Department of Integration of Chinese and Western Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao UniversityYantai, China; Emergency Centre, The Affiliated Yantai Yuhuangding Hospital of Qingdao UniversityYantai, China.
Frontiers in Pharmacology
|February 25, 2017
Summary
Carbon monoxide (CO) poisoning causes cognitive impairment. N-Butylphthalide (NBP) treatment improved cognitive function and protected brain tissue by balancing key protein expressions in rats.
Area of Science:
- Neuroscience
- Toxicology
- Pharmacology
Background:
- Cognitive impairment is a common neurological issue following carbon monoxide (CO) poisoning.
- N-Butylphthalide (NBP) has demonstrated potential neuroprotective effects in prior research.
Purpose of the Study:
- To investigate the efficacy of NBP in mitigating cognitive dysfunction induced by acute severe CO poisoning in a rat model.
- To explore the molecular mechanisms underlying NBP's neuroprotective effects.
Main Methods:
- Rats were exposed to CO to establish a poisoning model.
- Treatment groups received hyperbaric oxygen therapy, with one group additionally receiving NBP.
- Cognitive function, hippocampal ultrastructure, and protein expressions (calpain 1, CaMK II) were assessed using behavioral tests, electron microscopy, immunofluorescence, and western blot.
Main Results:
- CO poisoning led to significant cognitive impairment and hippocampal damage.
- Expressions of calpain 1 and CaMK II proteins were notably elevated post-CO exposure.
- NBP treatment improved cognitive function, preserved hippocampal ultrastructure, and reduced calpain 1 and CaMK II protein levels.
Conclusions:
- CO poisoning induces cognitive deficits through the upregulation of calpain 1 and CaMK II proteins.
- NBP administration offers neuroprotection by normalizing these protein expressions and maintaining hippocampal integrity.
- NBP shows promise as a therapeutic agent for brain injury resulting from CO poisoning.
Keywords:
CO poisoningCa2+/calmodulin dependent protein kinase IICalpain 1N-butylphthalidecognitive functionrat
