AIM To investigate whether ginsenoside Rg1 can reverse chronic lead-induced impairment of long-term potentiation (LTP) in the CA1 region of rat hippocampus. METHODS Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams whose drinking water (20 mL per day) contained 0.2% lead acetate. Field excitatory postsynaptic potentials (fEPSP) were recorded and LTP was induced in the CA1 region in rat hippocampal slices on postnatal 20-25 d. RESULTS In hippocampal slices from both control and lead-exposed rats, perfusion with ginsenoside Rg1 50 μmol·L-1 for 20 min induced enhancement of fEPSP (LTP), while the amplitude of LTP in lead-exposed rats was lower than that of controls. In hippocampal slices from chronic lead-exposed rats, LTP induced by high-frequency stimulation (HFS, 1s, 100 Hz) was significantly reduced, while perfusing with ginsenoside Rg1 (50 μmol·L-1) for 20 min increased the amplitudes of LTP induced by HFS by 47.1%. CONCLUSION Rg1 can increase basic synaptic transmission and partially reverse chronic lead-induced impairment of HFS-LTP.

Objective To explore the association between tumor necrosis factor receptor associated factor 6 (TRAF6) polymorphisms and the susceptibility to sepsis. Method Haplotype tagging single nucleotide polymorphisms (htSNPs) were selected from the HapMap database. The htSNPs were genotyped in 255 patients with sepsis and 260 control subjects by the Beckman SNP stream genotyping platform. The association with susceptibility to and severity of sepsis were estimated by logistic regression with adjustment for age, sex, smoking, drinking,chronic diseases status, APACHE Ⅱ score and critical illness. Results Of 13 TRAF6 ANPs, 7 were tagged by htSNPs. Of them, 5 htSNPs (rs5030496, rs5030411, rs5030416, rs5030445 and rs3740961) were used for final genotyping analysis. Genotype frequencies of those htSNPs were conformed to the Hardy-Weinberg law in both patients and controls. There were no significant association found between the 5 htSNPs and susceptibility to sepsis.Also, there was no significant association between the TRAF6 polymorphisms and the septic shock, death from sepsis as well as organ dysfunction. Conclusions The TRAF6 gene polymorphisms might not play a major role in severity of sepsis.