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- Xiaoming Liu, Xuan Yue, Shengzhi Chen, Jiao Chen, and Rui Li.
- Department of Neurology, Xuzhou Children's Hospital, Xuzhou, Jiangsu 221002, P.R. China.
- Exp Ther Med. 2015 Nov 1; 10 (5): 1784-1788.
AbstractIntactable epilepsy (IE) is relatively common in pediatric epilepsy. The resistance mechanism of IE has been previously investigated. Multidrug-resistant associated protein 1 (MRP1) and MRP2 are associated with drug transport. The aim of the present study was to investigate the expression of MRP1 and MRP2 in peripheral blood mononuclear cells of children with IE. Fifty outpatient or inpatient children were included in the study as the experimental group. Additionally, 50 children with epilepsy controlled by anti-epileptic drugs (AEDs) and 50 healthy children without epilepsy, who served as the control group, were included in the present study. Expression of MRP1 and MRP2 in the peripheral blood mononuclear cells of children in all the groups was detected using RT-PCR and western blot analysis. The results showed that the relative expression of MRP1 and MRP2 mRNA in the peripheral blood mononuclear cells of children with IE (MRP1, 0.795±0.042; MRP2, 0.804±0.023) was higher than that in epilepsy controlled by AEDs (MRP1, 0.682±0.030; MRP2, 0.675±0.021) and healthy children without epilepsy (MRP1, 0.665±0.031; MRP2, 0.654±0.029) (P<0.01). The mean relative expression of MRP1 and MRP2 protein in the peripheral blood mononuclear cells of children with IE (MRP1, 2.027±0.034; MRP2, 1.902±0.021) was higher than that in children with epilepsy controlled by AEDs (MRP1, 1.131±0.042; MRP2, 1.086±0.027) and healthy children without epilepsy (MRP1, 1.093±0.023; MRP2, 1.045±0.018) (P<0.01). The difference in the MRP1 and MRP2 mRNA and protein expression between the children with epilepsy controlled by AEDs and healthy children without epilepsy was not statistically significant (P>0.05). In conclusion, a higher expression of MRP1 and MRP2 in the peripheral blood mononuclear cells of children with IE may be relevant to the drug-resistant mechanism of IE.
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