RESUMEN
[Purpose] The purpose of this study was to analyze and compare electrophysiological characteristics observed in nerve conduction studies (NCS) of chronic inflammatory demyelinating polyneuropathy (CIDP) and Charcot-Marie-Tooth disease type 1 (CMT 1). [Subjects] A differential diagnosis of acquired and congenital demyelinating neuropathies was based on a study of 35 patients with NCS-confirmed CIDP and 30 patients with CMT 1 genetically proven by peripheral myelin protein-22 (PMP-22) gene analysis, pulsed-field gel electrophoresis (PFGE), and Southern blot analysis. [Methods] We analyzed values collected in motor nerve conduction studies. We conducted dispersion analysis of the amplitudes of the compound muscle action potential (CMAP) of various nerve types and correlation coefficient analysis of the motor nerve conduction velocity (MNCV). [Results] We found that CIDP and CMT 1 were clearly attributable to severe polyneuropathy. In dispersion analysis, CIDP showed greater differences in proximal-to-distal amplitude ratios. Moreover, CMT 1 showed relatively high correlations compared to CIDP based on correlation coefficient analysis of MNCV. [Conclusion] The results of this study suggest that CIDP showed greater asymmetry than CMT 1 in MNCV and CMAP amplitudes.
RESUMEN
Pectolinarin, [5,7-Dihydroxy 4',6-dimethoxyflavone 7-rutinoside, 7-[[6-O-(6-Deoxy-α-L-mannopyranosyl)-ß-D-glucopyranosyl] oxy]-5-hydroxy-6-methoxy-2-(4-ethoxyphenyl)-4H-1-benzopyran-4-one], has been stated one of the major compounds in Cirsium nipponicum (Maxim.) Makino. It is characterized by biological functions of hepatoprotective, anti-inflammatory and antiobesity activities. In this research, it was explained that pectolinarin causes apoptosis in PC12 cells conducted by DNA fragmentation and formation on apoptotic bodies through the activation of ER stress sensors (ATF6 fragmentation and eIF2α phosphorylation). The result of treating the PC12 cells with 50 µM pectolinarin for 24 h has come to increase ATF6 mRNA expression up to 1.6 times, PERK expression up to 1.7 times and IRE1 expression up to 1.4 times, respectively, compared to those of the control. ATF6 fragmentation by pectolinarin treatment was increased about 2 times compared with its control, and phosphorylation of eIF2α was increased 2.5 times. The results proposed that the perception of the molecular mechanisms underlying pectolinarin-caused apoptosis may be useful in new natural medicinal products and health supplements for the apoptosis-related diseases.