Rab7b Overexpression –Ameliorated Ischemic Brain Damage Following tMCAO Involves Suppression of TLR4 and NF-κB p65

In this study, by investigating a rat model with cerebral stroke, we foun d that Rab7b was upregulated in the rat brain following the transient middle cerebral artery occlusion (tMCAO). Functionally, overexpression of Rab7b in the brain by DNA transfection reduced cerebral infarction and improved neurological outcome following tMCAO, suggesting that Rab7b alleviates ische mic brain damage. Mechanistically, Rab7b overexpression suppressed the expression of TLR4 and NF-κB p65 and also inhibited the activation of NF-κB p65. Furthermore, Rab7b overexpression suppressed the production of proinflammatory mediators including TNF-α, IFN-γ, IL-1β, and IL-6 in the brain f ollowing tMCAO. In summary, these results suggest that Rab7b protects against ischemic brain damage following tMCAO and that this protection may relate to the suppressed inflammatory response mediated by TLR4 and NF-κB p65. Our study might offer Rab7b as a novel therapeutic target in the treatment of cerebral stroke.
Source: Journal of Molecular Neuroscience - Category: Neuroscience Source Type: research