Article Publish Status: FREE
Abstract Title:

BKchannel is a molecular target of vitamin C to protect against ischemic brain stroke.

Abstract Source:

Mol Membr Biol. 2019 Apr 16:1-25. Epub 2019 Apr 16. PMID: 30991005

Abstract Author(s):

Luyao Li, Shan Li, Chuanbing Hu, Li Zhou, Yujiao Zhang, Mingyan Wang, Zhi Qi

Article Affiliation:

Luyao Li


Epidemiological studies have demonstrated that vitamin C decreases the risk of stroke, which has generally been ascribed to its function as antioxidant and free radical scavenger. However, whether there is a defined molecular target for vitamin C on stroke is unknown. Utilizing middle cerebral artery occlusion (MCAO) in rats as a model for ischemic stroke, we demonstrated that long-term, low-dose administration of vitamin C prior to MCAO could exert significant neuroprotective effect on the brain damage. The long-term, low-dose vitamin C pre-treated rats had decreased brain infarct size and decreased neurological deficit score compared with the vehicle or single high dose pre-treated MCAO rats. Furthermore, electrophysiological experiments using patch clamp technique showed that vitamin C increased the whole-cell current of the large-conductance Ca-activated K(BK) channel. Moreover, vitamin C increased the open probability of the channel without change its amplitude. Importantly, blockade of the BKchannels abolished the neuroprotective effect of vitamin C on MCAO. Therefore, this study shows that long-term, low-dose pre-treatment with vitamin C could reduce MCAO-induced brain damage through activation of the BKchannels, suggesting that the BKchannel is a molecular target of vitamin C on stroke.

Study Type : Animal Study

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