Ischemic stroke accounts for almost 80% of the clinical stroke. Ischemic stroke cause severe brain inflammation, and pro-inflammatory cytokines secretion through the activation of toll-like receptor and inflammasome. Clinical studies indicate that the level of vitamin D concentration is associated with higher risk of stroke. However, the molecular mechanism is remain unclear. This study aimed to investigate the protective action of vitamin D on cerebral ischemia-reperfusion injury and the possible molecular mechanism. Eight-weeks-old male Sprague-Dawley rats were assigned to (1) control group (sham) ; (2) ischemia/reperfusion group (I/R) ; (3) vitamin D deficiency group (VDD group) : dietary deprivation of vitamin D for 14 days ; (4) vitamin D supplements group (VDS group) : 0.7μg /kg vitamin D supplements for 8 days. Middle cerebral artery occlusion (MCAO) was performed with SD rats, and 90 mins late to initiate reperfusion to investigate the effect of vitamin D supplements and deprivation to the brain damage and the performance of relational molecular. Results showed that vitamin D deficiency increased the severity of brain damage, lipid peroxidation products MDA accumulation and pro-inflammatory cytokines release. In contrast, vitamin D supplements improved brain damage. Western blot indicated that vitamin D deficiency may active TLR2-MyD88-NF-κB signaling cascade and NLRP3 inflammasome induce cleaved caspase-1 protein expression, increase IL-1β secretion. However, vitamin D can inhibit TLR2 and NLRP3-related protein expression. Besides, vitamin D can inhibit inflammation through the activation of TLR10-PI3K-AKT signaling pathway.In conclusion, Vitamin D might reduce cerebral ischemic-reperfusion oxidative damage and inflammation by inhibited activation of TLR2, reduced the mature of pro-inflammatory factor IL-1β and activation of TLR10 to protect against cerebral ischemia-reperfusion injury.
|Effective start/end date||2018/08/01 → 2021/07/31|
- Ischemic stroke
- Vitamin D
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