Pregnane X Receptor Not Nuclear Factor-kappa B Up-regulates P-glycoprotein Expression in the Brain of Chronic Epileptic Rats Induced by Kainic Acid

Neurochem Res. 2017 Aug;42(8):2167-2177. doi: 10.1007/s11064-017-2224-x. Epub 2017 Mar 16.

Abstract

Drug-resistance epilepsy (DRE) is attributed to the brain P-glycoprotein (P-gp) overexpression. We previously reported that nuclear factor-kappa B (NF-κB) played a critical role in regulating P-gp expression at the brain of the acute seizure rats. This study was extended further to investigate the interaction effect of NF-κB and pregnane X receptor (PXR) on P-gp expression at the brain of chronic epileptic rats treated with carbamazepine (CBZ). The chronic epileptic models were induced by the micro-injection of kainic acid (KA) into rats' hippocampus. Subsequently, the successful models were treated with different intervention agents of CBZ; PMA(a non-specific PXR activity inhibitor) or PDTC(a specific NF-κB activity inhibitor) respectively. The expression levels of P-gp and its encoded gene mdr1a/b were significantly up-regulated on the brain of KA-induced chronic epilepsy rats or the epilepsy rats treated with CBZ for 1 week, meanwhile with a high expression of PXR. The treatment of PMA dramatically reduced both PXR and P-gp expressions at the protein and mRNA levels in the chronic epilepsy brain. By compared to the epilepsy model group, the P-gp expression was not markedly attenuated by the inhibition of NF-κB activity with PDTC treatment, nevertheless with a decrease of NF-κB expression in this intervention group. Higher levels of proinflammatory cytokines(IL-1β, IL-6, TNF-α) were found both in the brain tissue and the serum in the epilepsy rats of each group. There was a declined trend of the pro-inflammatory cytokines expression of the PDTC treatment group but with no statistical significance. This study demonstrates for the first time that P-gp up-regulation is due to increase PXR expression in the chronic phase of epilepsy, differently from that NF-κB signaling may induce the P-gp expression in the acute seizure phase. Our results offer insights into the mechanism underlying the development of DRE using or not using CBZ treatment.

Keywords: Carbamazepine; Drug-resistant epilepsy; Nuclear factor-kappa B; P-glycoprotein; Pregnane X receptor.

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / biosynthesis*
  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / genetics
  • Animals
  • Brain / drug effects
  • Brain / metabolism*
  • Epilepsy / chemically induced
  • Epilepsy / genetics
  • Epilepsy / metabolism*
  • Gene Expression
  • Kainic Acid / toxicity*
  • Male
  • NF-kappa B / biosynthesis*
  • Pregnane X Receptor
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Steroid / biosynthesis*
  • Up-Regulation / drug effects
  • Up-Regulation / physiology

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • NF-kappa B
  • Pregnane X Receptor
  • Receptors, Steroid
  • Kainic Acid