ABSTRACT
Objective To investigate the role of nitric oxide/cyclic guanosine monophosphate (NO/ cGMP) signaling pathway in dexmedetomidine-induced reduction of neuropathic pain (NP) in the rats.Methods Forty-two healthy male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 7 groups (n =6 each) using a random number table:normal control group (C group);NP group;dexmedetomidine group (D group);dimethyl sulfoxide (DMSO) group;a non-selective nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) group (L-NAME group);inactive enantiomer D-NAME group (D-NAME group);a soluble guanylyl cyclase inhibitor 1H-[1,2,4] oxidazole[4,3-a] quinoxalin-1-one (ODQ) group (ODQ group).NP was induced by chronic constriction injury to the sciatic nerve in anesthetized rats.On day 7 after chronic constriction injury,dexmedetomidine 1.5 μg/kg was injected intrathecally in group D,and in DMSO,L-NAME,D-NAME and ODQ groups,DMSO l0 μl,L-NAME 100 μg,D-NAME 100 μg and ODQ 10 μg were injected intrathecally,respectively,and 25 min later dexmedetomidine 1.5 μg/kg was injected intrathecally.The thermal paw withdrawal latency was measured immediately after intrathecal administration and at 30,60,90,120,150,180 and 210 min after intrathecal administration,and the area under the curve of thermal paw withdrawal latency was calculated to reflect the thermal pain threshold.Results Compared with group C,the thermal pain threshold was significantly decreased in the other six groups (P＜0.05).The thermal pain threshold was significantly higher in D,DMSO,L-NAME,ODQ and D-NAME groups than in group NP (P＜0.05).Compared with group D,the thermal pain threshold was significantly decreased in L-NAME and ODQ groups (P＜0.05),and no significant change was found in the thermal pain threshold in D-NAME and DMSO groups (P＞0.05).Conclusion The mechanism by which dexmedetomidine reduces NP is related to activation of NO/cGMP signaling pathway in the rats.
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Objective To investigate the change of soluble P-selectin (sPsel)and von Willebrand factor (vWF)levels after ad-mission in traumatic patients and their relation with the coagulation indexes levels,coagulation disorders and prognosis.Methods 82 cases of severe trauma in ICU of Affiliated Tongji Hospital were prospectively selected and detected plasma sPsel,VWF anti-gen,protein C,activity of coagulation factor Ⅶ and routine coagulation indexes on admission and on every day within the first week after admission.The 30 d fatality rate was recorded.Results The sPsel and vWF levels on admission in the patients with coagula-tion disorders were lower than those in the patients without coagulation disorders (P <0.05)and significantly correlated with the coagulation indexes (protein C and coagulation factor Ⅶ)levels (P <0.05).The vWF level within 3 d after admission in the death patients was significantly lower than that in the survival patients,but which on 7 d after admission in the death patients was signifi-cantly higher than that in the survival patients (P <0.05 );no significant difference in sPsel level within 1 week after admission were found between the survival patients and the death patients.Conclusion Among severe traumatic patients in ICU,the low lev-els of sPsel and VWF on admission are associated with the coagulation disorders,the significant rise of vWF level on 7 d after ad-mission is associated with the increase of the 30 d fatality rate.
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Objective To determine whether anticoagulation markers can improve mortality prediction in patients of surgical intensive care unit (ICU).Methods A case-control study was adopted,252 patients from Tongji hospital's surgical ICU and 30 healthy control individuals were investigated.The protein C,antithrombin,thrombomodulin,and other coagulation/ inflammatory markers were detected.The Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score were obtained.Markers level comparison among survivors,non-survivors and controls were conducted with single factor variance analysis,Kruskal-Wallis test or Mann-Whitney U test.Results Between survivors and non-survivors after 28-day hospitalization,there were significant difference on protein C levels[(70.2 ±22.7)％ vs (48.6 ±29.8)％,t=2.84,P＜0.01],APACHE Ⅱ scores[(21.0±8.2) vs (29.5 ±10.9),t =-2.51,P＜0.05] and prothrombin times[(12.9-± 3.5) s vs (18.8 ± 10.2) s,t =-2.13,P ＜ 0.05].Combining protein C levels with APACHE Ⅱ score could obtain a higher mortality prediction efficiency in patients of surgical ICU than any single marker (AUC =0.806).That protein C concentration less than 47.5％ [OR =6.40,95％confidence interval(CI) 2.526-16.216,P ＜0.001] and APACHE Ⅱ score (OR =1.123,95％ CI 1.012 -1.250,P ＜ 0.05) were the independent risk factors for surgical ICU death.Conclusion Decrease of protein C levels predict increase of mortality risk in patients of surgical ICU,combining protein C with APACHE Ⅱ score can improve the prognostic accuracy for patients of surgical ICU.(Chin J Lab Med,2013,36:339-342)
ABSTRACT
To study the anticancer activities of curcumin on human hepatocarcinoma cell line Sk-hep-1 and its related molecular mechanism which has not been elucidated. In the present study,we showed that curcumin inhibited proliferation of Sk-hep-1 cells in a dose-dependent manner through MTF assay. The effect of curcumin on apoptosis in Sk-hep-1 cells was investigated by DAPI staining and the various apoptosis was observed in hepatocarcinoma cell lines Sk-hep-1, HepG2 and Hep3B, but not in normal liver cell line Chang's liver with curcumin treatment. Cell cycle analysis results showed that curcumin treatment resulted in dramatic accumulation of Sk-hep-1 cells at the G0/G1 or G2/M phase. The effect of curcumin on the expression of anti-apoptosis genes (Survivin and BCl-xL) and drug resistance genes (DRG2 and MDR1) was studied by reverse transcription-polymerase chain reaction (RT-PCR). The expression of MDR1 mRNA was significantly decreased in Sk-hep-1 cells treated with curcumin, while no alterations in the amount of DRG2 and anti-apoptosis genes' mRNA levels were found. These results indicate that curcumin is able to inhibit proliferation and induce apoptosis in Sk-hep-1 cells and it may cause by down-regulating the expression of MDR1 mRNA.