Effects of propofol on glutamatergic neuronal activity in paraventricular thalamus / 药学学报

This study explored the effects of propofol on the activity of glutamatergic neurons in the paraventricular thalamus (PVT) and the underlying mechanisms at the molecular level using whole-cell patch-clamp techniques. Acute brain slices containing the PVT were obtained from 8 weeks old C57BL/6J mice. The electrophysiological characteristics of PVT neurons were recorded in current-clamp mode, then single-cell sequencing was used to identify neuronal types. The firing frequencies before, during, and after propofol or intralipid application were recorded as FB, FD and FW; and the membrane potentials were recorded as MPB and MPD. Picrotoxin (PTX) was used to block inhibitory gamma-aminobutyric acid type A (GABAA) receptors during the application of propofol at 10 μmol·L-1. Then, GABAA receptor-mediated spontaneous and miniature inhibitory postsynaptic currents (sIPSCs and mIPSCs) were recorded, and the effects of 10 μmol·L-1 propofol were investigated. The animal experiments were approved by the Medical Animal Administrative Committee of Shanghai Medical College Fudan University. The results showed that there were no significant differences in FB, FD and FW during intralipid and 2 μmol·L-1 propofol application. With propofol at 5, 10 and 20 μmol·L-1, FD decreased significantly when compared with FB, and FW increased significantly as compared with FD (P < 0.01). The inhibition degree of the three concentration groups was significantly different (P < 0.01). In addition, with propofol at 20 μmol·L-1, MPD hyperpolarized significantly (P < 0.01). In the presence of PTX, 10 μmol·L-1 propofol could not suppress the firing frequency of PVT glutamatergic neurons. Propofol at 10 μmol·L-1 prolonged the decay time of sIPSCs (P < 0.01) and mIPSCs (P < 0.05), and increased the amplitude (P < 0.01) of mIPSCs of PVT glutamatergic neurons. Together, these results indicate that propofol can inhibit the activity of PVT glutamatergic neurons in a concentration-dependent and reversible manner, and the effect is likely to be mediated by postsynaptic GABAA receptors.

Placental Foxp3 expression in patients with preeclampsia and correlation of Foxp3 gene locus 924 (rs2232365) polymorphism with preeclampsia / 南方医科大学学报

<p><b>OBJECTIVE</b>To detect changes of Foxp3 expression in the decidua in patients with preeclampsia and investigate the correlation of Foxp3-924 (rs2232365) polymorphisms with preeclampsia.</p><p><b>METHODS</b>From October 2011 to December 2012, 252 normal pregnant women and 156 preeclampsia patients of Han nationality from the same geographic region were tested for Foxp3-924 genotypes by polymerase chain reaction with sequence-specific primer (PCR-SSP). Sixty-eight of the patients with preeclampsia (33 with mild and 35 with severe preeclampsia) and 30 of the normal pregnant women were also examined for Foxp3 expression in the decidua using immunohistochemical method.</p><p><b>RESULTS</b>Foxp3 positive expression rates in the decidua was 51.52% in mild preeclampsia and 28.57% in severe preeclampsia cases, significantly lower than that in the control group (86.67%, P<0.05). In preeclampsia patients, the frequencies of Foxp3-924G/G, G/A, and A/A genotypes were 0.1346, 0.4615 and 0.4038, respectively, and the frequencies of Foxp3-924A and Foxp3-924 G were 0.6346 and 0.3654, respectively. The genotype frequencies of Foxp3-924G/G, G/A and A/A in the control group were 0.1508, 0.4087 and 0.4405, respectively, and the frequencies of Foxp3-924 A and Foxp3-924 G were 0.6448 and 0.3552, respectively. No significant differences were found in the gene frequencies of Foxp3-924G/A between preeclampsia patients and the control group (P>0.05).</p><p><b>CONCLUSION</b>The expression level of Foxp3 in the placental tissue of preeclampsia patients is significantly lower than that in normal pregnant women, suggesting that lowered Foxp3 expression decreases the immunosuppressive function and causes imbalance of immune tolerance between maternal-fetal to induce preeclampsia. Foxp3-924 polymorphisms is not significantly correlated with the occurrence of preeclampsia.</p>

Effects of stellate ganglion block on blood pressure in spontaneously hypertensive rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effects of stellate ganglion block (SGB) on blood pressure in spontaneously hypertensive rats(SHRs).</p><p><b>METHODS</b>Thirty-two 10-week-old male spontaneously hypertensive rats(SHRs) were assigned randomly into four groups: left stellate ganglion block group(Group LS), right stellate ganglion block group(Group RS), captopril group(Group D) and control group(Group C). Arterial systolic blood pressure(SBP) was measured, and endothelin (ET-1) and endothelial nitric oxide synthase(eNOS) in blood vessels were detected by radioimmunoassay.</p><p><b>RESULTS</b>Compared with baseline value, the blood pressure of Group LS gradually increased significantly (P<0.05 or P <0.01); however, the blood pressure of Group RS was stable(P >0.05) and increased only at week 2(P <0.05).The blood pressure of Group D decreased significantly at week 2 and week 4, and it remained stable compared with baseline value (P<0.05). The blood pressure of Group C gradually increased at weeks 2-10, compared with baseline values (P <0.01). Compared with Group LS and Group C, the expression of eNOS in blood vessels of Group RS significantly increased (P <0.05), and ET-1 decreased (P <0.05).</p><p><b>CONCLUSION</b>The right stellate ganglion block can significantly lower blood pressure, down-regulate ET-1 and up-regulate eNOS protein expression.</p>

Protective effects of emulsified isoflurane after myocardial ischemia-reperfusion injury and its mechanism in rabbits / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To evaluate the protective effects of 8% emulsified isoflurane after myocardial ischemia-reperfusion injury and its mechanism in rabbits.</p><p><b>METHODS</b>Twenty-four male adult New Zealand white rabbits were anesthetized with intravenous injection of 30 mg/kg pentobarbital followed by 5 mg x kg(-1) x h(-1) infusion. All rabbits were subjected to 30 minutes of left anterior descending coronary artery (LAD) occlusion and 3 hours of subsequent reperfusion. Before LAD occlusion, the rabbits were randomly allocated into three groups for preconditioning treatment (eight for each group). The control group (C group) received intravenously 0.9% NaCl for 30 minutes. The emulsified isoflurane group (EI group) received 8% emulsified isoflurane intravenously till 0.64% end-tidal concentration for 30 minutes that was followed by a 15-minute washout period. The Intralipid group (IN group) received 30% Intralipid for 30 minutes. The infarcted area, plasma malondialdehyde (MDA) content, superoxide dismutase activity (SOD) and nitrite concentration after 3-hour myocardial perfusion were recorded simultaneously.</p><p><b>RESULTS</b>For the myocardial ischemia-reperfusion injury animals, the infarcted size in the EI group was significantly reduced (91.9% +/- 8%) as compared with control group (39% +/- 6%, t=5.19, P<0.01). The plasma SOD activity and nitrite concentration in EI group were significantly higher than those in control group (t=2.82, t=8.46, P<0.05), but MDA content was lower in EI group than that in control group (t=2.56, P<0.05).</p><p><b>CONCLUSIONS</b>The results indicate that emulsified isoflurane has a cardioprotection effect against ischemia-reperfusion injury. This beneficial effect of emulsified isoflurane is probably through NO release and consequently by increase in antioxidation of myocardium.</p>