DL‐3‐n‐butylphthalide alleviates vascular cognitive impairment by regulating endoplasmic reticulum stress and the Shh/Ptch1 signaling‐pathway in rats
Journal of Cellular Physiology
Published online on October 11, 2018
Abstract
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Abstract
Background
DL‐3‐n‐butylphthalide (NBP) has been approved to be effective in improving cognitive deficits. The aim of the current study was to determine whether NBP protects against cognitive deficits in a rat model of vascular dementia (VD) induced by chronic cerebral hypoperfusion (CCH) by regulating the sonic hedgehog (Shh)/patched1 (Ptch1) pathway and endoplasmic reticulum stress (ERS)‐related markers.
Methods
Adult male Sprague‐Dawley rats were subjected to permanent bilateral occlusion of the common carotid arteries (2VO) to established the model of VD. These rats were randomly divided into five groups: sham, model, NBP30 (30 mg/kg), NBP
60 (60 mg/kg), and NBP
120 (120 mg/kg) groups. The Morris water maze test was used to assess for cognitive function at 4 weeks after operation.
Results
NBP significantly alleviated spatial learning and memory impairment, and inhibited the loss of neurons in the CA1 region of the hippocampus. Western blot analysis and real‐time quantitative polymerase chain reaction analysis revealed that plasticity‐related synaptic markers and the Shh/Ptch1 pathway significantly increased in the NBP treated groups, while ERS‐related markers decreased.
Conclusion
The results of the current study prove that the Shh/Ptch1 pathway plays an essential role in the model of VD. NBP had protective effects on cognitive impairment induced by CCH. This mechanism was associated with ERS and the Shh/Ptch1 pathway. Meanwhile, the Shh/Ptch1 pathway and ERS may interact with each other.
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