Abstract
Aryl hydrocarbon receptor (AhR) antagonism can mitigate cellular damage associated with cerebral ischaemia and reperfusion (I/R) injury. This study investigated the neuroprotective effects of AhR antagonist administration before reperfusion in a rat stroke model and influence of the timing of AhR antagonist administration on its neuroprotective effects. Magnetic resonance imaging (MRI) was performed at baseline, immediately after, and 3, 8, and 24 h after ischaemia in the sham, control (I/R injury), TMF10 (trimethoxyflavone [TMF] administered 10 min post-ischaemia), and TMF50 (TMF administered 50 min post-ischaemia) groups. The TMF treatment groups had significantly fewer infarcts than the control group. At 24 h, the relative apparent diffusion coefficient values of the ischaemic core and peri-infarct region were significantly higher and relative T2 values were significantly lower in the TMF10 groups than in the control group. The TMF treatment groups showed significantly fewer terminal deoxynucleotidyl transferase dUTP nick-end labelling positive (+) cells (%) in the peri-infarct region than the control group. This study demonstrated that TMF treatment 10 or 50 min after ischaemia alleviated brain damage. Furthermore, the timing of AhR antagonist administration affected the inhibition of cellular or vasogenic oedema formation caused by a transient ischaemic stroke.
Highlights
In acute stroke patients, restoring blood supply as soon as possible is considered the optimal treatment to preserve neurological function
There was no significant difference in regional cerebral blood flow (rCBF) reduction (P > 0.05) and the sum of relative apparent diffusion coefficient (rADC) values among the TMF10, TMF50, and control groups (P > 0.05)
We evaluated the neuroprotective effects of Aryl hydrocarbon receptor (AhR) antagonism before reperfusion and assessed the relationship between the timing of AhR antagonist administration and subsequent protective effects against cerebral ischaemia and reperfusion (I/R) injury in rats
Summary
In acute stroke patients, restoring blood supply as soon as possible is considered the optimal treatment to preserve neurological function. After effective thrombolytic therapy for stroke, cerebral ischaemia and reperfusion (I/R) injury can occur and cause more severe secondary damage to brain tissue[2]. To modulate neuronal damage due to transient cerebral artery occlusion in vivo (Fig. 1A)[10,11]; it was demonstrated that early inhibition of AhR conferred neuroprotection in ischaemic stroke, whether inhibition was effective at later time points has not been revealed. We investigated the neuroprotective effects of AhR antagonism before reperfusion in a rat model of stroke induced by transient middle cerebral artery occlusion (tMCAO) and reperfusion. We used in vivo magnetic resonance imaging (MRI) and histochemical analyses to assess whether the timing of AhR antagonist administration influences its neuroprotective effects
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