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Fig. 1 | Cell & Bioscience

Fig. 1

From: TRIM67 alleviates cerebral ischemia‒reperfusion injury by protecting neurons and inhibiting neuroinflammation via targeting IκBα for K63-linked polyubiquitination

Fig. 1

The expression of TRIM67 decreased after cerebral ischemia‒reperfusion injury. A and B RT-qPCR (A) and western blotting (B) assays showing Trim67 mRNA and protein expression in mouse peri-infarct cortex, hippocampus and striatum tissues at the specified periods following middle cerebral artery occlusion/reperfusion (MCAO/R) (n = 5). C Quantification of TRIM67 expression normalized to that of β-actin in B. D Representative double immunostaining of TRIM67 (red) with NeuN (a neuronal marker, green), Iba-1 (a microglial marker, green) and GFAP (an astrocyte glial marker, green) from ischemic penumbra of brain tissue after MCAO surgery. EG Quantification of TRIM67 fluorescence intensity in NeuN-, Iba1-, and GFAP-positive cells were quantified using ImageJ. The analytical graph was presented as normalized to the sham group. Scale bars, 40 μm. (n = 5). The mean ± SD are displayed for all data. **p < 0.01, ***p < 0.001 and ****p < 0.0001

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