| Objective:To explore the expression level and mechanism of participation of TLR2 Protein in ischemic cerebral white matter dysmylination in Beagle dogs.Methods:16 adult beagles were divided into control group(group A)and the experimental group by the principle of randomization.Which the experimental group were divided into B,C and D group,based on the different degree in beagle cerebral ischemic mode of vascular ligation.To examine the white matter in the peripheral ventricle edge of the laboratory animal as test sample.The pathological changes and standardized scores of The degree of white matter demyelination lesions in each group were observed by using the HE stain and LFB staining.TLR2 、NG2 and CNPase expression levels were detected in samples by immunohistochemical methods.Spearman rank correlation analysis was used to analyze the correlation between TLR2 and CNPase.Results:(1)In the control group observes uniform dyeing in wihte matter,nerve fiber in alignment,normal form of cells;The experimental group B/C/D show different degrees of uneven dyeing,disordered arrangement of nerve fibers,cell swelling and nuclear pyknosis.LFB staining were visible normal myelin sheath form,dyeing uniformity in control group;The experimental groups show obviously demyelinating changes:myelin disorder and uneven dyeing in group B;myelin swelling or fracture and obvious vacuole formation in group C;disappeared myelinated fibers、forming lipid vacuoles and vacant colour in group D.(2)The level of demyelination was assessed using the Hideaki standardized score,which the lowest score was 0.63±0.52 in the control group,the score of experimental group B and C was 1.25±0.46 and 1.63±0.52,the highest score was 1.88±0.64 in group D.The comparison between the control group and the group B,C and D was statistically significant(P < 0.05).(3)Immunohistochemical testing revealed:1)TLR2 protein expression levels: The level of expression was lowest at 0.148 + 0.058 in control group,then The experiment group B and C was 0.185±0.023 and 0.185±0.025,the highest level of expression was 0.191±0.016 in group D.Compared with the control group,the expression of the TLR2 protein in B,C,and D was significantly higher and the difference was statistically significant(P < 0.05).2)NG2 expression : The level of expression was lowest at 0.147±0.021 in control group,then The experiment group B andC was 0.169±0.017 and 0.170±0.016,the highest level of expression was 0.177±0.018 in group D.Compared with the control group,the expression of the NG2 in B,Cand D was significantly higher and the difference was statistically significant(P < 0.05).3)CNPase expression levels: The level of expression was highest at 0.287±0.032 in control group,however the lowest level of expression was 0.213±0.015 in group D,The experiment group B and C was 0.225±0.025 and0.222±0.02.Compared with the control group,the expression level of CNPase was decreased in the B,C and D groups,and the difference was statistically significant(P < 0.05).(4)The expression of TLR2 and CNPase was shown by Spearman rank correlation analysis: The expression level of TLR2 and CNPase was negatively correlated(r =-0.382,P < 0.01).Conclusion:The TLR2 protein involved in the demyelination lesion of chronic ischemic white matter.The mechanism may be a rise in the expression level of the TLR2 protein,which on the one hand causes the CNPase to be lowered and the reduction of the oligodendrocytes,on the other hand obstructs the mature of oligodendrocyte precursor cells and affects the myelin regeneration,so induces demyelination lesion. |
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