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Objective To investigate the role of ceramide in radiation induced bystander effect (RIBE) in vivo by irradiating Caenorhabditis elegans with proton microbeam.Methods The posterior pharynx of wide-type N2 and genetically mutated L4-staged worms was irradiated with 2 000 particles,then germ cell apoptosis and gene expression were analyzed.Results Point-fixed radiation to posterior pharynx of N2 worms significantly increased the number of apoptotic germ cells (t =9.007,P<0.05),but not in the worms with deletion mutants of ceramide synthase (CerS) genes (hyl-1 and lagr-1) (P>0.05).Realtime quantitative PCR assay indicated that in both N2 and lagr-1 (gk327);hyl-1 (ok976) worms,the genes of egl-1 and ced-13 in core apoptosis pathway were up-regulated after radiation to posterior pharynx,without statistical significance between these two strains (P>0.05).The gene expression levels of hyl-1 and lagr-1 were increased in both N2 and hus-1 (op241) worms after radiation with no statistical significant difference between two strains (P>0.05).Furthermore,radiation-induced germ cell apoptosis was increased in abl-1 (ok171) worms (t=13.241,P<0.05),rather than in lagr-1(gk327);hyl-1(ok976);abl-1(ok171) worms (t=13.462,P<0.05).Conclusions Ceramide is required for RIBE on germ cell apoptosis in C.elegans,and it might play function together with egl-1 and ced-13 in core apoptosis pathway and HUS-1 in DNA damage response pathway.But ceramide had antagonistic relationship with anti-apoptotic protein abl-1 in germ cell apoptosis.
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To explore the effect of long-time propofol infusion on myocardial enzymes, mitochondrial cytochrome C and ATP in rabbits. Methods: A total of 18 New Zealand rabbits were randomly divided into 3 groups: a control group, a propofol group and an intralipid group. The rabbits were continuously infused with 0.9% normal saline in the control group, 1% propofol in the propofol group, and 10% intralipid in the intralipid group, respectivey. The arterial blood was collected at 0, 8, 16 h and the end of experiment to examine creatine kinase (CK) and creatine kinase isoenzyme (CK-MB). In the end, the myocardial mitochondria from myocardial tissues was separated by differential centrifugation, and mitochondrial cytochrome C content and adenosine triphosphate (ATP) levels were examined by high performance liquid chromatography. Results: Compared with the control group, the release of cytochrome C from mitochondria were increased in the propofol group and the intralipid group (both P0.05). There was also no significant difference in the ATP content of the mitochondria among the 3 groups (P>0.05). The levels of CK were increased at 8, 16 and 24 h after infusion in the propofol group and the intralipid group compared with that before the infusion (all P0.05); compared with the control group, the levels of CK-MB were obviously increased in the infusion of propofol for 24 h in the propofol group (P<0.05). Conclusion: The levels of serum CK increase after the infusion of propofol and intralipid for a long time, and the levels of CK-MB also elevate in the infusion of propofol. Propofol and intralipid can increase the release of myocardial mitochondrial cytochrome C, but they don't affect the ATP production in myocardial mitochondrial.
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Animales , Conejos , Adenosina Trifosfato , Metabolismo , Creatina Quinasa , Sangre , Metabolismo , Forma MB de la Creatina-Quinasa , Sangre , Metabolismo , Citocromos c , Metabolismo , Emulsiones , Farmacología , Infusiones Intravenosas , Mitocondrias , Miocardio , Química , Fosfolípidos , Farmacología , Polifosfatos , Propofol , Farmacología , Aceite de Soja , FarmacologíaRESUMEN
Objective To investigate the protective effect of NS398,a specific cyclooxygenase-2 inhibitor,on microglial activation-mediated neuronal damage.Methods The microglia of neonatal SD rat were isolated and cultured in the medium containing 1 μg/ml of LPS.The morphological changes of microglial were observed.The IL-1β and TNF-α levels were detected by Western blot in LPS group (group L) and control group (group C).The hippocampal neurons of neonatal SD rats were cultured in the control medium (group C),LPS-activated microglial conditioned medium (group L) and LPS-activated microglial conditioned medium with NS398 (group N),respectively.The survival rate of neurons were detected by MTT.The respiration of hippocampus neurons was determined by detecting the ratio of lactic acid/pyruvic acid.Results LPS-induced microglial activation was characterized by the morphological change and increased secretion of IL-1β and TNF-α.The survival rate of neurons cultured by microglia activated conditioned medium was 64.37%,while the group N was 80.25% (P<0.01).In group L,the ratio of lactic acid/pyruvic acid (27.34±8.53) was significantly higher than that of group N (20.32±6.05,P<0.01) and group C (14.95±4.72,P<0.01).Conclusion NS398,a specific cyclooxygenase-2 inhibitor,has a protective effect on rat hippocampus neuron damaged by activated microglia.
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Objective To investigate the impact of the COX-2 specific inhibitor parecoxib on postoperative serum cytokines and early cognitive function in the elderly patients undergoing knee replacement.Methods Seventy-two elderly patients undergoing knee replacement were divided into a control group (group Ⅰ)and parecoxib group (group Ⅱ).MMSE score were compared at preoperative 1 d and postoperative 1 d,3 d,7 d.Before induction of anesthesia (T1 ),postoperative 6 h (T2 ),1 d (T3 ),3 d (T4 ),7 d (T5 ),the serum IL-1β,IL-6 concentrations were measured,meanwhile the serum S-100βwere measured in T2 .Results At postop-erative 1 d,3 d,the MMSE score in group Ⅰ was significantly lower compared with the preoperative (P <0.05).IL-6 in T2 ,IL-1βin T3 increased in both group.In group Ⅱ,three days later,the exaltation of plasma inflammatory factors returned to the preopera-tive level,but this process last untill T5 in group Ⅰ.The plasma concentration of IL-6 in T2 ,T3 ,T4 and IL-1βin T3 ,T4 in group Ⅰwere higher than group II (P <0.05).At T2 ,the serum S-100βin group Ⅰ was (1 625 ± 364)pg/mL higher than group Ⅱ(1 263 ±174)pg/mL(P <0.05).Conclusion The protective effection of COX-2-specific inhibitor parecoxib upon postoperative cognitive decline in elderly patients undergoing orthopedic surgery may be related to inhibition of peripheral cytokine release.
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Objective To observe the preventive efficacy and safety of dexmedetomidine with parecoxib sodium on the patients with postoperative hyperalgesia induced by remifentanil. Methods A total of 100 female patients undergoing elective surgery under general anesthesia were as-signed into four groups according to the table of random number:the control group (group C),the parecoxib sodium group (group P),the dexmedetomidine group (group D)and the parecoxib sodium combined with the dexmedetomidine group (group DP).The vital signs were monitored and the total intravenous anesthesia was performed.All the patients were give intravenous injection of 0.2μg·kg-1 ·min-1 remifentanil and 4-12 mg·kg-1 ·h-1 propofol to maintain the anesthesia.Patients in group P were given 40 mg parecoxib sodium 30 minutes before the end of the operation.Patients in group D were give intravenous injection of 0.6μg·kg-1 ·min-1 dexmedetomidine consistently till 30 min before the end of the operation.Patients in group DP were given 0.6 μg·kg-1 ·min-1 till 30 min before the end of the operation and were given 40 mg parecoxib sodium.The VAS scores were re-corded at 1,2,6,12,24 hours.The cases of agitation,rigors,nausea and vomiting and increasing of analgesics were recorded.Results The postoperative VAS scores in group P,group D and group DP were significantly lower than group C(P <0.05).The postoperative VAS scores in group DP were significantly lower in group P and group D (P<0.05).Cases of agitation and rigors in group D and group DP were less than group C(P <0.05).The increasing of analgesics in group DP was much higher than other groups(P<0.05).Conclusion After induced,patients were given intravenous in-jection of 0.6 μg·kg-1 ·min-1 dexmedetoniding consistently till 30 min before the end of the opera-tion were given 40 mg parecoxib sodium can effectively prevent hyperalgesia after remifentanil anes-thesia without significant increase in revival time and obtain a better sedation.
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Objective To get minimally invasive and cosmetic effect,minimal incision was used in thyroid surgery.Methods By using MPBS series instruments,thyroid surgeries were performed through anterior cervical tiny incision approach.Results 164 cases of subtotal theroidectomy and 78 cases of thyroid individual lobe resection were performed.The length of incision were(2.0 ± 0.5)cm,and the duration of operation time were(40 ± 10)min.the volume of blood loss were(30 ± 10)ml.There was no conversion to traditional open operation.After 3 years follow-up,short and long term complications were not found.Conclusions Minimally incision thyroid surgery has advantages of less trauma,cosmetic effect and does not compromise the safety.The disadvantages of this method is limited operative field and inconvenience for operation,which need to be further improved.
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Objective To investigate the role of intercellular adhesion molecule-1(ICAM-1)in Isoflurane against hepatic ischemia-reperfusion(I/R)injury in vivo.Methods Thirty-two female SD rats were randomly divided into 4 groups:sham-operation group(A),I/R group(B),Isoflurane group(C),I/R+ Isoflurane group(D).Groups A and C were be used as controls.In groups B and C,the hepatic hilar vessels distributing to the left and median lobes were clamped to induce partial hepatic ischemia(70%).Reperfusion was done 60 min after hepatic ischemia.The animals were killed 3 h after reperfusion,then the specimens of liver tissues and blood were obtained.ALT and AST in blood serum were detected as liver damage markers.The histological examination of liver tissues was done by hematoxylin and eosin staining.The levels of ICAM-1 protein in the hepatic tissues were detected by immunohistochemistry.Results After hepatic ischemia-reperfusion,the ICAM-1 protein expression in the hepatic tissues increased;ALT and AST increased;Reperfusion induced severe liver damage.Isoflurane significantly inhibited the ICAM-1 expression.Conclusion The degree of hepatic ischemia-reperfusion injury is closely associated with the expression level of ICAM-1.Isoflurane abates liver ischemia-reperfusion injury and inhibits the ICAM-1 expression.