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Objective To evaluate the effects of pulsed radiofrequency (PRF) application to dorsal root ganglia on the expression of interferon regulatory factor 8 (IRF8) in the spinal cord and brain-derived neurotrophic factor (BDNF) protein in the nucleus accumbens of rats with neuropathic pain (NP).Methods Forty healthy pathogen-free male Wistar rats,weighing 180-200 g,aged 2 months,were divided into 4 groups (n=10 each) using a random number table:sham operation group (group Sham),group NP,sham PRF group (group SPRF) and PRF group.NP was induced by chronic constriction injury (CCI) to the left sciatic nerve of anesthetized rats.The mechanical paw withdrawal threshold (MWT) was measured before CCI and at 3,7,10,14,21,28,35 and 42 days after CCI.Sucrose preference test and forced-swim test were performed at 42 days after CCI for determination of the expression of IRF8 in the spinal cord and BDNF in the nucleus accumbens by Western blot.Results Compared with group Sham,the MWT at each time point after CCI and rate of preference for sucrose were significantly decreased,the duration of immobility in forced-swim test was prolonged,and the expression of IRF8 and BDNF was up-regulated in NP,SPRF and PRF groups (P＜0.05).Compared with group NP,the MWT at 10-42 days after CCI and rate of preference for sucrose were significantly increased,the duration of immobility in forced-swim test was shortened,and the expression of IRF8 and BDNF was down-regulated in group PRF (P＜0.05),and no significant changes were found in the parameters mentioned above in group SPRF (P＞O.05).Conclusion The mechanism by which PRF application to dorsal root ganglia alleviates NP and depressive-like behaviors is probably related to down-regulation of the expression of IRF8 in the spinal cord and BDNF in the nucleus accumbens of rats.
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Objective To determine the median effective concentration (EC50) of epidural lidocaine inhibiting herpetic neuralgia.Methods The patients with thoracic or lumbar herpetic neuralgia,aged 20-60 yr,with body mass index of 18-25 kg/m2,of ASA physical status Ⅰ or Ⅱ,were included in the study.Epidural catheter was placed under the guidance of the digital subtraction angiography (DSA).An injection of iohexol mixed with lidocaine was given under the guidance of DSA to make sure that drug solution covered all the injured nerve roots.The initial concentration of lidocaine was 0.37％.The concentration was determined by up-and-down sequential allocation.Each time the concentration of lidocaine increased/decreased in the next patient depending on whether or not the analgesia was effective.The ratio between the two successive concentrations was 1.06.Effective analgesia was defined as VAS score ≤ 1 within 30 min after administration.The EC50 and 95 ％ confidence interval of lidocaine inhibiting herpetic neuralgia were calculated using Dixon formula.Results The EC50 of lidocaine inhibiting herpetic neuralgia was 0.199 ％ and the 95 ％ confidence interval was 0.168 ％-0.216 ％.Conclusion The EC50 of epidural lidocaine required to inhibit herpetic neuralgia is 0.199％.
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Objective To evaluate the role of phosphatase and tensin homolog deleted on ehromo-some ten (PTEN) protein in sevoflurane postconditioning-induced mitigation of focal cerebral ischemia-reperfusion (I/R) injury via activating PI3K/Akt pathway in rats.Methods One hundred and eight Sprague-Dawley rats,aged 2-3 months,weighing 250-280 g,were randomly assigned into 6 groups (n =18 each) using a random number table:sham operation group (group S),group I/R,I/R + sevoflurane postconditioning group (group I/R + S),I/R + normal saline group (group I/R + NS),I/R + selective PTEN inhibitor pic group (group I/R + P),and I/R + pic + sevofluraue postconditioning group (group I/R + P+ S).Focal cerebral I/R was induced by right middle cerebral artery occlusion (MCAO).The animals were anesthetized with intraperitoneal chloral hydrate.In I/R + P and I/R + P + S group,pic 20 μg/100 g (0.4 ml/100 g) was injected intraperitoneally every 3 h for 4 times before MCAO,and the equal volume of normal saline was given instead of pic in I/R + NS group.The rats in all sevoflurane postconditioning groups inhaled 2.5 ％ sevoflurane for 30 min starting from the onset of reperfusion,and the rats in the other groups inhaled oxygen for 30 min instead.At 24 h of reperfusion,neurological deficit scores (NDSs) were measured and the rats were then sacrificed.Their brains were removed for determination of infarct size (by TTC),cell apoptosis (by TUNEL),and expression of phosphorylated PTEN (p-PTEN) protein and phosphorylated Akt (p-Akt) (by Western blot).Apoptosis index was calculated.Results Compared with S group,the NDSs,percentage of cerebral infarct size and apoptosis index were significantly increased,and the expression of p-Akt and p-PTEN protein was up-regulated in the other 5 groups.Compared with I/R and I/R + NS groups,the NDSs,percentage of cerebral infarct size and apoptosis index were significantly decreased,and the expression of p-Akt and p-PTEN protein was up-regulated in I/R + S,I/R + P and I/R + P + S groups.There were no significant changes in the parameters mentioned above between I/R + S,I/R + P and I/R + P + S groups,and between I/R and I/R + NS groups.Conclusion Sevoflurane postconditioning can activate PI3K/Akt pathway via inhibiting PTEN protein,thus mitigating focal cerebral I/R injury in rats.
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Objective To investigate the protective effects of cardiomyopeptidin (CMP) pretreatment against hippocampal neuronal injury caused by anoxia-reoxygenation and the underlying mechanism. Methods Hippocampal neurons were isolated from neonatal SD rats and cultured for 9-10 days. The cultured primary hippocampal neurons were randomly divided into 4 groups: ( I ) control group; ( II ) anoxia-reoxygenation group (A-R); (I) CMP 10?g?ml-1 group (CMP1) and (IV) CMP 100 ?g?ml-1 group (CMP2). In A-R group hippocampal neurons were subjected to 4 h anoxia (cultured in 95 % N2 + 5 % CO2 ) and 48 h reoxygenation (cultured in aerobic environment). In group III and IV CMP was added to culture media with end-concentration of CMP 10 ?g?ml-1 or 100?g?ml-1 before oxygen-deprivation. Neuronal viability was assessed by MTT method and Bcl-2 protein expression was determined by immune-cytochemistry.Results The optical density (OD) value of hippocampal neurons and the Bcl-2 expression were significantly higher in group IV (CMP2) than those in group Q (A-R) and III (CMP1) (P
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Objective To determine what effects diazoxide, a selective opener of mitochondrial ATP-sensitive potassium channel ( Mito-KATP ), exerts on apoptosis in hippocampal neurons caused by anoxia-reoxygenation.Methods Newborn SD rats (
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Objective To investigate the effects of propofol on the survival rate of and the expression ofinducible nitric oxide synthase (iNOS) in the cultured hippocampal neurons.Methods Hippocampal neuronsisolated from new-born SD rats were dispersed and cultured in B27 culture medium for 9-10days.The culturedhippocampal neurons were randomized to one of 4 groups: (1)control group; (2) anoxia group; (3)propofol 4?g?ml~(1) + anoxia group; (4) propofol 12 ?g?ml~(-1)+ anoxia group. For anoxia the cultured hippocampal neurons wereplaced in a tightly closed vessel filled with 95 % N_2～5% CO_2 at 37℃ for 4h,followed by 24 h reoxygenation. Inthe propofol groups (group 3 and 4) propofol was added before anoxia. Survival rates were measured by MTTassay The levels of iNOS expression were determined by immunocytochemistry method.Results In the twopropofol groups (group 3 and 4) propofol attenuated the levels of iNOS expression in the cultured hippocampalneurons and increased the survival rates as compared with anoxia group (group 2). Depofol reduced the levels ofiNOS expression in a concentration-dependent manner.Conclusion Propofol can decrease the level of iNOSexpression in cultured hippocampal neurons induced by anoxia-reoxygenation and increase the survival rate ofhippocampal neuron after anoxia-reoxygenation. Inhibition of iNOS expression may explain partly the mechanism ofcerebral protective effects of propofol.