Protective Effect of Dl-3n-butylphthalide on Learning and Memory Impairment Induced by Chronic Intermittent Hypoxia-Hypercapnia Exposure

Abstract

Cognitive impairment is a common finding in patients with chronic obstructive pulmonary disease (COPD), but little attention has been focused on therapeutic intervention for this complication. Chronic intermittent hypoxia hypercapnia (CIHH) exposure is considered to be responsible for the pathogenesis of COPD. Dl-3n-Butylphthalide (NBP), extracted from Apium graveolens Linn, has displayed a broad spectrum of neuroprotective properties. Our study aimed to investigate the potential of NBP on CIHH-induced cognitive deficits. The cognitive function of rats after CIHH exposure was evaluated by the Morris water maze, which showed that the NBP treated group performed better in the navigation test. NBP activated BDNF and phosphorylated CREB, the both are responsible for neuroprotection. Additionally, NBP decreased CIHH induced apoptosis. Moreover, NBP further induced the expression of HIF-1α, accompanied by the up-regulation of the autophagy proteins Bnip3, Beclin-1 and LC3-II. Finally, NBP also reversed the decreased expression of SIRT1 and PGC-1α, but the expression of Tfam, Cox II and mtDNA remained unchanged. These results suggested that the neuroprotective effects of NBP under CIHH condition possibly occurred through the inhibition of apoptosis, promotion of hypoxia-induced autophagy, and activation of the SIRT1/PGC-1α signalling pathway, while stimulation of mitochondrial biogenesis may not be a characteristic response.

Effects of calcitriol on experimental spinal cord injury in rats

“…Previous studies have shown that Bcl2 exerts an antiapoptotic effect, 15 whereas Bax participates in the induction of apoptosis; 16 activation of C-caspase3 is seen as a hallmark of apoptotic cell death, acting as the final executor of apoptosis. 17 In the present study, western blotting analyses indicated lower levels of both C-caspase3 and Bax, whereas expression of Bcl2 was increased, in the calcitriol group relative to the SCI group. Furthermore, both immunohistochemistry for C-caspase3 and TUNEL staining showed significant decreases in the number of apoptosis-positive cells in the spinal cord lesions of calcitriol-treated rats.…”

Paeoniflorin attenuates hippocampal damage in a rat model of vascular dementia

“…Bcl-2 and Bax are two primary genes responsible for the regulation of apoptotic cell death, and their individual products possess opposing functions (24). Bcl-2 is functionally characterized as the apoptosis-suppressing factor, whereas Bax is considered as the apoptosis-promoting factor (25).…”

Novel Treatment Strategies for the Nervous System: Circadian Clock Genes, Non-coding RNAs, and Forkhead Transcription Factors

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