Abstract
Treating cerebral ischemia continues to be a clinical challenge. Studies have shown that the neurovascular unit (NVU), as the central structural basis, plays a key role in cerebral ischemia. Here, we report that anthocyanin, a safe and natural antioxidant, could inhibit apoptosis and inflammation to protect NVU in rats impaired by middle cerebral artery occlusion/reperfusion (MCAO/R). Administration of anthocyanin significantly reduced infarct volume and neurological scores in MCAO/R rats. Anthocyanin could also markedly ameliorate cerebral edema and reduce the concentration of Evans blue (EB) by inhibiting MMP-9. Moreover, anthocyanin alleviated apoptotic injury resulting from MCAO/R through the regulation of Bcl-2 family proteins. The levels of inflammation-related molecules including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), which were over-expressed with MCAO/R, were decreased by anthocyanin. In addition, Nuclear factor-kappa B (NF-κB) and the NLRP3 inflammasome pathway might be involved in the anti-inflammatory effect of anthocyanin. In conclusion, anthocyanin could protect the NVU through multiple pathways, and play a protective role in cerebral ischemia/reperfusion injury.
Highlights
Treating cerebral ischemia continues to be a clinical challenge and underlying mechanisms of cerebral ischemia remain elusive
Behavioral assessment showed that anthocyanin significantly decreased the neurological severity scores and attenuated cognitive function decline measured by novel object recognition test of middle cerebral artery occlusion/reperfusion (MCAO/R) rats in a dose-dependent manner (Figures 1C,E,F)
The results showed that compared with the sham rats, MCAO/R significantly up-regulated the expression of TNFα, IL-1β, and IL-6 in the cerebral cortex, and anthocyanin significantly inhibited the expression of tumor necrosis factor-α (TNF-α), IL-1β, and IL-6 (Figure 4A)
Summary
Treating cerebral ischemia continues to be a clinical challenge and underlying mechanisms of cerebral ischemia remain elusive. Recent studies have demonstrated that in response to cerebral ischemia, NLRP3 inflammasomes promote inflammatory responses in neurons and glial cells, resulting in tissue damage (Gao et al, 2017). Studies have shown that activation of the NLRP3 inflammasome in brain cells can regulate the activation of caspase-1, which converts pro-IL-1β into a mature form of IL-1β (Tong et al, 2015). Given these complex mechanisms, the efficacy of a single target drug in the treatment of stroke may not be satisfactory, and, it is necessary to identify a pleiotropic drug. We investigated the protective effects of anthocyanin in rats with MCAO/R injury, and found some clues on the underlying mechanism of protection
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