Toad urothelium barrier is the model to mimic and investigate urothelium permeability. Thiazide blocked ionic transportation in polarized membrane state. Jellyfish venom causes pores to be adjusted to urothelium permeability which improved polarization. This study aimed at CfTX-1 peptide in urothelium permeability evoked polarizations. Thiazide pretreated toad urothelium permeability to ions were investigated in modified Ussing chamber. Thiazide urothelium were further intervened by CfTX-1 peptide and treated with G-protein receptor agonists. 0.1 mol CaCl2 activated transurothelium potential differences were recorded by unipolar lead and computerized by fast Fourier transform technique. Apical chamber was settled as anode. The amplitude of potential differences were evaluated to determine the urothelium polarizations. The results indicated that CaCl2 activation induced a positive monophasic wave in thiazide urothelium, which suggested the urothelium was slightly polarized and significantly enhancive in adrenergic receptor treated urothelium. Furthermore, CfTX-1 peptide enhanced transurothelium potential difference in thiazide urothelium, therefore, urothelium were supra polarized. NPPB treatment significantly attenuated this supra polarization, which suggested that the Cl- influx was the main stream ionic compound of this polarization. It is concluded that CfTX-1 peptide was considered to generate supra polarization in thiazide urothelium. This mechanism is useful to study the improvement of drug delivery crossing urothelium barrier.
Key words: CfTX-1 partial sequence, toad urothelium, supra polarization, Cl- permeability.
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