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Objective To evaluate the efficacy of ultrasound-guided anterior quadratus lumborum block combined with general anesthesia for laparoscopic radical resection of rectal carcinoma. Methods A total of 80 patients of both sexes, of American Society of Anesthesiologists physical status Ⅰ or Ⅱ, aged 40-64 yr, scheduled for elective laparoscopic radical resection of rectal carcinoma, were divided into 2 groups ( n=40 each) using a random number table method: anterior quadratus lumborum block combined with general anesthesia group ( group QG) and general anesthesia group ( group G) . In group QG, anteri-or quadratus lumborum block was performed with 0. 33％ ropivacaine 25 ml and dexamethasone 5 mg under ultrasound guidance before operation, and the same procedure was performed on the other side. Combined intravenous-inhalational anesthesia was applied, propofol 3-5μg∕ml and remifentanil 3-5 ng∕ml were given by target-controlled infusion, and cisatracurium was intermittently injected in two groups. Patient-controlled intravenous analgesia with sufentanil 2μg∕kg was used for postoperative analgesia. The analgesic pump was set up to deliver a 2 ml bolus dose with a 15-min lockout interval. Bruggrmann comfort scale ( BCS) scores were recorded at 1, 6, 12, 24 and 48 h after operation ( T1-5 ) . Tramadol was used for rescue analgesic after operation. The consumption of remifentanil and sufentanil, requirement for tramadol, occurrence of adverse reactions and patients' satisfaction with postoperative analgesia were recorded. The emergence time, first ambulation time, time to first flatus∕poo and length of hospital stay were also recorded. The develop-ment of anterior quadratus lumborum block-related complications was recorded. Results Compared with group G, BCS scores were significantly increased at T4,5 , the consumption of remifentanil, requirement for tramadol and incidence of nausea and vomiting were decreased, patients' satisfaction with postoperative an-algesia was increased, and the emergence time, first ambulation time, time to first flatus∕poo and length of hospital stay were shortened in group QG (P<0. 05). Conclusion Ultrasound-guided anterior quadratus lumborum block combined with general anesthesia can reduce the consumption of opioids in the perioperative period and is helpful in improving outcomes when used for laparoscopic radical resection of rectal carcinoma.
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Objective To evaluate the role of phosphatidylinositol 3?kinase(PI3K)∕serine?threo?nine kinase(Akt)signaling pathway in propofol?induced invasion of human liver cancer cell line HepG2. Methods HepG2 cells were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum in a 5% CO2incubator at 37℃. HepG2 cells at the logarithmic growth phase were divided into 6 groups(n=18 each)using a random number table: control group(group C), propofol group(group P), PI3K∕Akt signaling pathway agonist IGF?1 group(group IGF), PI3K∕Akt signaling pathway inhibitor LY294002 group(group LY), IGF?1 plus propofol group(group IGF+P)and LY294002 plus propofol group (group LY + P). Propofol 120 μg∕ml was added in group P. IGF?1 10 nmol∕L was added in group IGF. LY294002 10 μmol was added in group LY. In group IGF+P, 10 nmol∕L IGF?1 was added, cells were in?cubated for 24 h, and then 120 μg∕ml propofol was added. In group LY+P, 10 μmol LY294002 was add?ed, cells were incubated for 24 h, and then 120 μg∕ml propofol was added. The invasion of cells was measured by Transwell invasion assay at 24 h of incubation. The expression of PI3K and Akt mRNA in cells was determined by real?time polymerase chain reaction. The expression of Akt, PI3K and phosphorylated Akt(p?Akt)was detected by using Western blot. Results Compared with group C, the invasive cell count was significantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was decreased, and the expression of Akt mRNA was down?regulated in P, P+IGF, LY and P+LY groups, and the invasive cell count was significantly increased, the expression of PI3K protein and mRNA was up?regulated, p?Akt∕Akt ratio was increased, and the expression of Akt mRNA was up?regulated in group IGF(P<0.05). Compared with group P, the invasive cell count was significantly increased, the expression of PI3K protein and mRNA was up?regulated, p?Akt∕Akt ratio was increased, and the expres?sion of Akt mRNA was up?regulated in group P+IGF, and the invasive cell count was significantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was decreased, and the ex?pression of Akt mRNA was down?regulated in group P+LY(P<0.05). The invasive cell count was signifi?cantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was de?creased, and the expression of Akt mRNA was down?regulated in group P+IGF as compared with group IGF (P<0.05)and in group P+LY as compared with group LY(P<0.05). Conclusion The mechanism by which propofol inhibits invasion of HepG2 cells is related to inhibiting activation of PI3K∕Akt signaling path?ways.
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Objective To investigate the effects of sevoflurane on HIF-1α/epithelial mesenchymal transition (EMT)pathway activity and invasion of lung cancer in rats undergoing one lung ventilation (OLV). Methods Lung cancer model of SD rats was established. Rats were randomly divided into 4 groups:group control(group C), group two lungs ventilation(TLV)(group T),group one lungs ventilation(group O),and group sevoflurane +one lungs ventilation(group SO). Two lung ventilation was performed after endotracheal intubation for 2.5 h in group T. OLV was performed after endotracheal intubation for 2 h in group O and SO. The end-expiratory concentration of sevoflurane of rats in group SO was maintained 2.6% during OLV period. Left lung cancer tissues were harvested at 0.5 h of TLV. The protein levels of HIF-1α,Vimentin and Fibronectin in lung cancer were determined by Western blot. The mRNA levels of MMP-2 and MMP-9 in lung cancer were evaluated by RT-PCR. Results The expres-sions of HIF-1α,Vimentin,Fibronectin,MMP-2,and MMP-9 in group O and group SO were significantly higher than those in group C and group T(P<0.05). The expressions of HIF-1α,Vimentin,Fibronectin,MMP-2,and MMP-9 were decreased significantly in group SO as compared with group O(P<0.05). Conclusion Sevoflurane inhibits the elevation of HIF-1α/EMT pathway activity and invasion ability induced by OLV.
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Objective To observe the protective effect of dexmedetomidine(Dex)at different doses com-bined with ulinastatin in lung resection patients with one lung ventilation. Methods 80 patients having undergone unilateral lung resection were divided into four groups randomly:control group(C group)and groups Dex 1-3,20 cases in each group.One lung ventilation(OLV)was used in all the groups during operation.The patients in groups Dex 1-3 were treated with 0.5,1.0,2.0 μg/kg combined with ulinastatin,and the C group with amount of normal sa-line instead.The comparisons were done among the four groups in terms of SOD,L-6,IL-10,serum malondialde-hyde(MDA)concentration at 5 min after endotracheal intubation(T0),30 min(T1),60 min(T2),120 min (T3)as well as the levels of FVC,FEVl and FEVl/FVC at 24 h,48 h and 72 h after surgery. Results In the groups C and Dex 1,SOD decreased at T1-4 and IL-6,MDA and IL-10 at T2-4 rose.SOD decreased at T2-4 in groups Dex 2-3 and MDA,IL-6 and IL-10 rose.Compared with group C,the levels of SOD and IL-10 at T2-4 in groups Dex 1-2 and at T1-4 in group Dex 3 rose. In groups Dex 1-3,postoperative FVC,FEVl and FEVl/FVC rose.Compared with group Dex 1 or 2 respectively,SOD and IL-10 at T2-4 in group Dex 3 significantly rose,but MDA and IL-6 significantly declined;FVC,FEVl and FEVl/FVC significantly rose 48 h and 72 h after surgery (P<0.05). Conclusion Dex combined with ulinastatin has a protective effect for patients with one lung ventila-tion after lung resection,with the best-suggested dose of 1.0 μg/kg.
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Objective To observe the effect of intrathecal injection of TRESK overexpression adenoviruson phosphorylation of JNK and apoptosis of neurons in neuropathic pain rats.Methods Seventy-two male SD rats were randomly divided into six groups:groups C,S,NP,T,V,and NS,12 for each group.SNI was administrated to rats in groups NP,T,V and NS.TRESK adenovirus and negative virus were intrathecally injected after use of SNI in groups T and V,while equal volume of NS was injected to rats in group NS.MWT and TWL were measured at 1 day before operation(baseline,BL)and at 1,3,7 and 14 days after operation (days 1,3,7,and 14).Six rats in each group were sacrificed at D7 to determinate the expression of TRESK protein of DRG.The other rats were sacrificed at D14 to determinate neural apoptosis and the expressions of caspase3 and p-JNK of DRG.Results As compared with groups C,S and T,the expression of TRESK protein was significantly decreased at D7 in groups NP,NS and V (P＜0.05).Compared with groups C and S,MWT was significantly decreased at days 1,3,7 and 14 (P＜0.05),phosphorylation of JNK in DRG was significantly increased at D14 (P＜0.05),neuronal apoptosis rate and expressions of Caspase3 of DRG were significantly increased at D14 (P＜0.05) in groups NP,T,NS and V.Compared with groups NP,V and NS,MWT was significantly increased at time points of days 1,3,7 and 14 in group T (P＜0.05),phosphorylation of JNK of in DRG was significantly decreased at D14 in group T (P＜0.05),neuronal apoptosis rate and expression of Caspase3 of DRG were significantly decreased at D14 in group T (P＜0.05).Intrathecal injection ofpAd/CMV/VS-DEST-TRESK obviously reduced mechanical hyperalgesia,upregulated TRESK expression,and lowered JNK phosphorylation and NP in SNI rat.Conclusions Intrathecal injection of TRESK over expression adenovirus relieves NP via inhibiting JNK activation and neuronal apoptosis.
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Objective To evaluate the effect of ultrasound-guided transverse abdominal plane block (TAPB) on postoperative analgesia in patients undergoing orthotopic liver transplantation under general anesthesia.Methods Forty American Society of Anesthesiologists physical status Ⅲ-V patients,with body mass index of 18-24 kg/m2,aged 18-64 yr,undergoing elective modified piggy-back orthotopic liver transplantation,were divided into 2 groups (n =20 each) by a random number table method:TAPB combined with general anesthesia group (TAPB-GA group) and general anesthesia group (GA group).In TAPB-GA group,two-point TAPB was performed below bilateral costal margins under ultrasound guidance after induction of general anesthesia,and a mixture of 0.33％ ropivacaine 15 ml plus 0.5％ dexamethasone 0.5 ml was injected into each point.The equal volume of normal saline was injected into each point instead in group GA.Patient-controlled intravenous analgesia was performed with sufentanil 2 μg/kg after operation in both groups.Sufentanil 5 μg was intravenously injected as rescue analgesic,and the visual analog scale score was mainrained ≤3 within 48 h after operation.The intraoperative consumption of remifentanil and extubation time after operation were recorded.The requirement for sufentanil as rescue analgesic and development of nausea and vomiting,itching and respiratory depression were recorded within 48 h after surgery.Results Compared with group GA,the intraoperative consumption of remifentanil and requirement for sufentanil as rescue analgesic within 48 h after surgery were significantly reduced,the time of extubation was shortened,and the incidence of nausea and vomiting,itching and respiratory depression was decreased in group TAPB-GA (P＜ 0.05).Conclusion Ultrasound-guided TAPB can provide better efficacy of postoperative analgesia with fewer adverse reactions in patients undergoing orthotopic liver transplantation under general anesthesia.
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Objective To observe the effects of sevoflurane pretreatment on lung metastasis of mouse Lewis lung cancer (LLC)cells.Methods Mouse LLC cells were inoculated in culture plate. After being cultured for 24 h the cells were randomly divided into four groups:group control (CC), group 1% sevoflurane (SC1),group 2% sevoflurane (SC2),and group 3% sevoflurane (SC3).Cells of group SC1-3 were exposed to 1%,2%,3% sevoflurane for 4 h respectively,cells of group CC were exposed to 95%O 2-5%CO 2 mixture air,and were then cultured for another 24 h.The invasive activity of cells was determined by Transwell assay.The migration of cells was evaluated by wound scratch assay.The expression of MMP-2 and MMP-9 in cells were detected by ELISA.Thirty-two C57BL/6 mice were divided into four groups (n = 8):group control (CM),group 1% sevoflurane (SM1),group 2% sevoflurane (SM2),and group 3% sevoflurane (SM3).LLC cells of group SC1-3 were injected into caudal vein of mouse in group SM1-3 respectively.Cells of group CC were injected into mouse of group CM.Lung metastasis inhibitory rates were evaluated after 3 weeks. Results Compared with group CC,the invasive activity and migration of cells in group SC1-3 were decreased significantly,group SC1 >group SC2 >group SC3 (P group SC2>group SC3 (P <0.05).Compared with group CM,lung metastasis inhibitory rates of group SM1-3 were increased significantly,group SM1 < group SM2 < group SM3 (P < 0.05 ). Conclusion Sevoflurane can inhibit the lung metastasis of mouse LLC cells,which maybe through down-regulating the expression of MMP-2 and MMP-9 in mouse LLC cells.
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Objective To evaluate the role of interleukin-4 receptor (IL-4R) in renal fibrosis following renal ischemia-reperfusion (I/R) injury in mice.Methods Twelve male wild type BALB/C mice and 12 IL-4Rα gene-knockout mice,aged 8-10 weeks,weighing 20-30 g,were used in the study.The mice of either type were divided into 2 groups (n =6 each) using a random number table:sham operation group (group S) and group I/R.In group I/R,renal I/R was induced by occlusion of the right renal artery for 1 h with atraumatic microclips followed by 2 weeks of reperfusion.The right renal artery was only isolated in group S.At 2 weeks of reperfusion,blood samples were taken from the orbital vein for determination of the concentrations of serum blood urea nitrogen (BUN) and creatinine (Cr).The renal tissues were obtained,and the renal fibrosis area was measured by Sirius Red staining.The expression of fibronectin (FN),collagen Ⅰ (COL-Ⅰ) and α-smooth muscle actin (α-SMA) in renal tissues was detected by immunofluorescence.The expression of signal transducer and activator of transcription 6 (STAT6) and phospho-STAT6 in renal tissues was determined by Western blot.The ratio of phoshop-STAT6 to STAT6 was calculated to reflect the phosphorylation of STAT6.Results Compared with group S of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly increased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly up-regulated,and the phosphorylation of STAT6 in renal tissues was significantly increased in group I/R of wild type and IL-4Rα KO mice (P＜0.05).Compared with group I/R of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly decreased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly down-regulated,and the phosphorylation of STAT6 in renal tissues was significantly decreased in group I/R of IL-4RαKO mice (P＜0.05).Conclusion The mechanism of renal fibrosis following renal I/R injury is partially related to IL-4R,and IL-4R results in renal fibrosis through promoting activation of STAT6 signaling pathway in mice.
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Objective To evaluate the effect of resveratrol on the activity of NADPH oxidase during acute lung injury induced by intestinal ischemia-reperfusion (I/R) in rats.Methods Thirty-two pathogenfree healthy female Sprague-Dawley rats,weighing 180-230 g,were divided into 4 groups (n =8 each) using a random number table:sham operation group (Sham group),intestinal I/R group (I/R group),vehicle group (Veh group) and resveratrol group (Res group).Intestinal I/R was produced by occlusion of the superior mesenteric artery for 75 min followed by 4 h of reperfusion.In group Res,resveratrol 15 mg/kg was intraperitoneally injected for 5 consecutive days before establishment of the model and at 15 min before ischemia.The equal volume of vehicle (0.5％ alcohol) was intraperitoneally injected in group Veh.The equal volume of normal saline was intraperitoneally injected in Sham and I/R groups.At the end of reperfusion,the rats were sacrificed and the lung was removed for microscopic examination of pathologic changes which were scored and for determination of wet/dry weight ratio (W/D ratio),malondialdehyde (MDA) content and superoxide dismutase (SOD) activity (by colorimetric method) and expression of NADPH oxidase subunits (gp91phox and p47phox) in lung tissues (by Western blot).Results Compared with group Sham,pathologic scores,W/D ratio and MDA content were significantly increased,the expression of gp91phox and p47phox was up-regulated,and the activity of SOD was decreased in I/R and Veh groups (P＜0.05).Compared with I/R and Veh groups,pathologic scores,W/D ratio and MDA content were significantly decreased,the expression of gp91phox and p47phox was down-regulated,and the activity of SOD was increased in group Res (P＜0.05).Conclusion The mechanism by which resveratrol reduces intestinal I/R-induced acute lung injury is related to inhibiting NADPH oxidase-mediated oxidative stress response of rats.
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Objective To evaluate the effect of oxycodone on migration of human colon cancer cells and the role of μ and κ receptors.Methods The human colon cancer HCT116 cells at the logarithmic growth phase were seeded in 24-well or in 6-well plates at a density of 1 × 106 cells/mnl (0.5 ml/well or 2 ml/well,144 wells in total).The cells were divided into 6 groups (n=24 each) using a random number table:control group (group C),1,5 and 10 μmol/L oxycodone groups (group O1,group O2 and group O3),oxycodone plus μ receptor antagonist CTOP group (group O2+CTOP) and oxycodone plus κ receptor antagonist nor-binaltorphimine group (group O2+BNI).The cells were incubated for 24 h with oxycodone 1,5 and 10 μmol/L in O1,O2 and O3 groups,respectively.The cells were incubated for 24 h with 5 μmol/L oxycodone plus 20 μmol/L CTOP and 5 μmol/L oxycodone plus nor-binahorphimin 20 μmol/L in O2+CTOP and O2+BNI groups,respectively.The invaded and migrated cells were counted,and the levels of Ras homolog gene family member A (RhoA),Rho-associated protein kinase 1 (ROCK1),matrix metalloproteinase-2 (MMP-2) and MMP-9 were detected.Results Compared with group C,the number of invaded and migrated cells was gradually decreased,and the levels of RhoA,ROCK1,MMP-2 and MMP9 were gradually decreased in O1,O2 and O3 groups (P＜0.05),and no significant change was found in the parameters mentioned above in group O2+BNI (P＞0.05).Compared with group O2,the number of invaded and migrated cells was significantly increased,and the levels of RhoA,ROCK1,MMP-2 and MMP9 were increased in group O2 + BNI (P＜0.05),and no significant change was found in the parameters mentioned above in group O2+CTOP (P＞0.05).Conclusion Oxyc odone can inhibit the migration of human colon cancer cells,and the mechanism is totally related to inhibition of RhoA/ROCKl signaling pathway activation after activating κ receptors,but not related to μ receptors.
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Objective To investigate the effects of post-operative analgesia with oxycodone or morphine for patients undergoing colon cancer radical surgery on platelet activation and cellular immunity.Methods Forty colon cancer patients scheduled for radical surgery, 23 males and 17 females, ASA physical status Ⅰ or Ⅱ, were randomly divided into 2 groups (n=20 each): oxycodone group (group O) and morphine group (group M).Patient-controlled intravenous analgesia (PCIA) was used for post-operative analgesia.PCIA solution contained oxycodone 1 mg/kg and tropisetron 6 mg in 100 ml normal saline in group O or morphine 1 mg/kg and tropisetron 6 mg in 100 ml normal saline in group M.Blood samples were obtained from the patients at 5 min before anesthesia induction (T0), 4 h after surgery (T1), 24 h after surgery (T2) and 48 h after surgery (T3).The levels of glycoprotein (GP)Ⅱb/Ⅲa, P-selection (CD62P), natural killer (NK) cells, NKT cells, and natural Treg (nTreg) cells were detected.The platelet aggregation rate (PAR) was determined.Results Compared with T0, the levers of GPⅡb/Ⅲa, CD62P, PAR and nTreg cells were significantly higher at T1 in group O and at T1, T2 in group M (P<0.05).Compared with T0, the levels of NK and NKT cells were decreased significantly at T1 in group O and at T1-T3 in group M (P<0.05).The levels of GPⅡb/Ⅲa, CD62P, PAR and nTreg cells at T2 and T3 in group O were decreased significantly as compared with group M (P<0.05).The levels of NK cells, NKT cells at T2 and T3 in group O were significantly higher than those in group M.Conclusion Post-operative analgesia with oxycodone for patients undergoing colon cancer radical surgery exhibits a more significant effect of decreasing platelets activity and presents a less disturbance on cellular immunity as compared with morphine.
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Objective To compare the anesthetic efficacy of ketamine and sevoflurane for foreskin ligation in the pediatric patients.Methods A total of 120 pediatric patients,aged 2-6 yr,weighing 10-18 kg,scheduled for elective foreskin ligation,were equally and randomly divided into ketamine group (group K) and sevoflurance group (group S).In group K,atropine 0.25 mg/kg and ketamine 2 mg/kgwere injected intravenously,and foreskin ligation was performed after loss of eyelash reflex.In group S,8％ sevoflurance was inhaled using the tidal volume technique,the concentration inhaled was adjusted to 4％ after loss of eyelash reflex,and then foreskin ligation was performed.The occurrence of crying before and during anesthesia induction,induction time,emergence time,occurrence of agitation during emergence from anesthesia and duration of agitation were recorded.Results Compared with group K,the rate of crying was significantly decreased,the emergence time was shortened (P＜0.05),and no significant difference was found in the induction time,incidence of agitation during emergence from anesthesia,and duration of agitation in group S (P＞0.05).Conclusion Sevoflurance provides better anesthetic efficacy than ketamine when applied for foreskin ligation in the pediatric patients.
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Objective To investigate the role of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) protein in the spinal cord neurons in diabetic neuropathic pain (DNP) in rats.Methods Male Sprague-Dawley rats,aged 2 months,weighing 180-200 g,were studied.Diabetes mellitus was induced by single intraperitoneal injection of streptozotocin (STZ) 60 mg/kg.Sixteen rats with DNP were randomly divided into 2 groups (n =8 each) using a random number table:DNP group and DNP+PTEN inhibitor bpv (pic) group (DPN-bpv group).Another 16 rats were equally and randomly divided into either control group (group C) or bpv group.In DNP-bpv and bpv groups,bpv (pic) 0.2mg/kg was injected intraperitoneally once a day within 14-28 days after injection of STZ.Before STZ injection (T1),and at 2,7,14,21 and 28 days after STZ injection (T2-6),the mechanical paw withdrawal threshold (MWT) was measured.After measurement of MWT,the rats were sacrificed,and the lumbar segments of the spinal cord (L4.5) were removed for determination of PTEN protein activity (by ELISA) and Akt (s473) phosphorylation (by Western blot).Results Compared with group C,the MWT was significantly decreased at T4-6,and the PTEN protein activity and Akt (s473) phosphorylation were significantly increased in DNP and DNP-bpv groups (P＜0.05 or 0.01).Compared with group DNP,the MWT was significantly increased at T6,and the PTEN protein activity and Akt (s473) phosphorylation were significantly decreased in group DNP-bpv (P＜0.05).Conclusion PTEN protein in the spinal cord neurons is involved in the maintenance of DNP in rats.
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Objective To investigate the effects of serum from patients receiving isoflurane and sevoflurane on the invasion and migration ability of human lung adenocarcinoma cell line A549. Methods Twenty ASAⅠorⅡ lung cancer patients aged 40 ~ 68 yr undergoing radical surgery were randomly divided into sevoflurane group (SEV group, n = 10) and isoflurane group (ISO group, n = 10). The concentration of sevoflurane or isoflurane maintained 1.5 MAC during anesthesia. Ten healthy volunteers were selected as control group. Serum was separated from blood sample taken at the end of surgery. A549 cells were randomly divided into sevoflurane group (group SEV, n = 10), isoflurane group (group ISO, n = 10) and control group (group C, n = 10). Cells of SEV group and ISO group were treated with 10% serum as respect to anesthetics for 24 hours. Cells of group C were treated with serum of control group. The invasion ability of cells was evaluated by Transwell assay. The migration ability of cells was determined by wound healing assay. The expressions of MMP-2 and MMP-9 in A549 cells were detected by ELISA. Results Compared with group C and ISO group,the number of invasive cells in group SEV was reduced significantly (P < 0.05). The levels of MMP-2 and MMP-9 in group SEV were significantly decreased compared with those of group C and ISO group (P<0.05). Conclusion The serum of patients receiving sevoflurane anesthesia can attenuate the metastatic ability of A549 cells through inhibiting the expression of MMP-2 and MMP-9.
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Objective To investigate the effects of sevoflurane and propofol on postoperative cognitive function after abdominal surgery for elderly patients with diabetes. Methods Seventy diabetic patients (aged 60~75 yr, ASAⅠorⅡ) underwent abdominal surgery and are included in the research. Diabetic patients were randomly divided into two groups (n=35): sevoflurane group(group DS) and propofol group (group DP). MMSE score, the attachment test, words memory test and Stroop color word test were carried and the results were recorded before operation (T1), postoperative 24 h (T2), 48 h (T3) and 1 w (T4). Results Compared with T1, patients′ MMSE score reduced at T2 and T3. Time spent in attachment test is longer at T2 and T3. Mistaken incidences in Stroop color words test 1, 2 and 3 are higher and time longer at T2. Time spent on Stroop color words test 2 and 3 is longer in T3. Words memory test reveals decline at T2 and T3, whose difference is statistically significant (P 0.05). Conclusion Sevoflurane and propofol can result in postoperative cognitive dysfunction for elderly patients with diabetes within 48 h after abdominal surgery, there were no difference between the effects of them.
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Objective To evaluate the role of T?type calcium channels in up?regulation of spinal Ca2+∕calmodulin?dependent protein kinase Ⅱ ( CaMKⅡ) expression in rats with neuropathic pain. Meth?ods Forty?eight male Sprague?Dawley rats, weighing 230-270 g, in which intrathecal catheters were suc?cessfully implanted, were divided into 4 groups ( n=12 each) using a random number table: sham opera?tion group (group S), neuropathic pain group (group NP), normal saline group (group NS), and T?type calcium channel blocker mibefradil group ( group M ) . The model of neuropathic pain was established by chronic compression of the dorsal root ganglion ( DRG) . Normal saline 20μl and mibefradil 200μg ( dilu?ted to 20μl in normal saline) were injected intrathecally at 5 days after compression of the DRG in NS and M groups, respectively. Before intrathecal catheter implantation ( T1 ) , before compression of the DRG ( T2 ) , at 5 days after compression of the DRG and before intrathecal administration ( T3 ) , and at 30, 60, 120 and 240 min after intrathecal administration ( T4?7 ) , the mechanical paw withdrawal threshold ( MWT) and thermal paw withdrawal latency ( TWL) were measured. The rats were sacrificed after the last measure?ment of the pain threshold at T7 , and the lumbar enlargement segments of the spinal cord were harvested for determination of CaMKⅡ expression by Western blot. Results Compared with group S, the MWT was significantly decreased, and TWL was significantly shortened at T3?7 , and the expression of spinal CaMKⅡ was significantly up?regulated in NP and M groups (P0.05). Conclusion T?type calcium channels are opened, the intra?cellular free calcium ion concentrations are increased, and activated spinal CaMKⅡ is involved in the de?velopment of neuropathic pain in rats.
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Objective To observe the effect of adenosine monophosphate activated protein kinase (AMPK) on attenuating inflammation in fibrosis induced hy acute ischemia reperfusion injury (IRI) in mice.Methods Forty eight male C57BL/6 mice were randomly divided into four groups:sham operation group (sham group),IRI group,AMPK inhibitor+IRI group (AMPK/IRI group) and normal saline+IRI group (NS/IRI group),12 mice each group.The mice with renal IRI were occluded for 30 min through clipping bilateral renal pedicle,then released renal perfusion.Mice in sham group were performed the separation of renal pedicle without clipping.Mice in AMPK/IRI group and NS/IRI group were respectively intraperitoneal injected AMPK inhibitor and normal saline before IRI.At the 2 d after operation,6 randomly-selected mice from each group were blooded by extraction eyeball to detect BUN and Scr.The renal histopathological changes were observed through HE staining.The mRNA expression of IL-1β,IL-6 and TNF-α was detected by real time PCR,and the level of AMPK phosphorylation was detected by Western blotting.At the 14 d after operation,Collagen 1 (COL1),α-SMA and fibronectin (FN) were detected by immunofluorescence and Western blotting in 6 remained mice from each group.The degree of kidney fibrosis was observed through sirus red staining.Results Compared with those in sham group,tubular interstitial damage was aggravated (P ＜ 0.05),BUN and Scr were increased (P ＜ 0.05),the mRNA expression of IL-1β,IL-6 and TNF-α was increased at the 2 d after operation (all P ＜ 0.05),and the level of AMPK phosphorylation was activated in IRI group and NS/IRI group (all P ＜ 0.05);the degree of kidney fibrosis and the expression of COL1,α-SMA and FN were increased obviously at the 14 d (all P ＜ 0.05).Compared with those in IRI group,in AMPK/IRI group tubular interstitial damage was aggravated (P ＜ 0.05),BUN and Scr were increased (all P ＜ 0.05),the mRNA expression of IL-1β,IL-6 and TNF-α was increased at the 2 d (all P ＜ 0.05),and the level of AMPK phosphorylation was decreased (P ＜ 0.05).Moreover,the degree of kidney fibrosis and the expression of COLI,α-SMA and FN were increased obviously at the 14 d in AMPK/IRI group (all P ＜0.05).Conclusions AMPK can ameliorate the acute renal ischemia reperfusion injury induce fibrosis in mice,and the mechanism may be related to the decrease of inflammatory reaction.
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Objective To investigate the effect of propofol on human renal tubule epithelial cell (HK-2 cells) fibrosis induced by ATP depletion/recovery and the role of transforming growth factor β activated kinase 1 (TAK1) in it.Methods HK-2 cells were seeded in 96-well plates,and randomly divided into 4 groups (n =36 each) using a random number table:control group (group C),ATP depletion/recovery group (group D/R),propofol group (group P),and TAK1 over-expression group (group T).HK-2 cells were exposed to antimycin A for 1 h and then returned to normal culture medium to establish the model of ATP depletion/recovery-induced injury.At 1 h before ATP depletion,the cells were incubated for 1 h in the DMEM liquid culture medium containing propofol with the final concentration of 20 μmol/L in group P,and the cells were incubated for 1 h in the DMEM liquid culture medium containing propofol with the final concentration of 20 μmol/L and TAK1 with the titer of 2× 107 TU/ml in group T,and the other treatments were similar to those previously described in group D/R.At 12 h after ATP recovery,the cell viability was evaluated by methyl thiazolyl tetrazolium assay,and cell apoptosis was detected using TUNEL and scored.The expression of TAK1 was detected using Western blot at 12,24 and 48 h after ATP recovery.The expression of α-smooth muscle actin (αSMA),fibronectin (FN),and collagen protein 1 (COL1) was measured at 48 h after ATP recovery.Results Compared with group C,the cell viability was significantly decreased,the apoptosis score was increased,and the expression of TAK1,COL1,αSMA and FN was up-regulated after ATP recovery in D/R,P and T groups (P＜0.05).Compared with group D/R,the cell viability was significantly increased,the apoptosis score was decreased,and the expression of TAK1,COL1,αSMA and FN was down-regulated after ATP recovery in P and T groups (P＜0.05).Compared with group P,the cell viability was significantly decreased,the apoptosis score was increased,and the expression of TAK1,COL1,αSMA and FN was up-regulated after ATP recovery in group T (P＜ 0.05).Conclusion Propofol can reduce HK-2 cell fibrosis induced by ATP depletion/recovery,and the mechanism may be related to down-regulation of TAK1 expression.
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Objective To investigate the role of chemokine CXC-ligand 16 (CXCL16) in renal ischemia-reperfusion (I/R) injury in the mice.Methods Twelve healthy male C57BL/6 mice and 12 CXCL16-knockout (CXCL16-KO) mice,aged 8-10 weeks,weighing 20-30 g,were studied.The 12 C57BL/6 mice were randomly divided into 2 groups (n=6 each) using a random number table:C57BL/6 sham operation group (group C-S) and C57BL/6 I/R group (group C-I/R).The 12 CXCL16-KO mice were randomly divided into 2 groups (n=6 each) using a random number table:CXCL16-KO sham operation group (group KO-S) and CXCL16-KO I/R group (group KO-I/R).The right kidney was removed,and the left kidney was exposed,and the renal artery was then clamped for 45 min with atraumatic microclips followed by 24 h reperfusion to establish the model of renal I/R in anesthetized mice.Venous blood samples were taken at 24 h of reperfusion for determination of the serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.The renal specimens were obtained at 24 h of reperfusion for microscopic examination of the pathological changes,and the damage to the renal tubules was scored.The number of myeloperoxidase (MPO) positive cells (MPO+ cells),F4/80+ cells and CD3+ cells in renal tissues was counted by immunohistochemistry.The expression of tumor necrosis factor-alpha (TNF-α),interleukin-1beta (IL-1β),IL-6,and macrophage inflammatory protein-2 (MIP-2) mRNA in renal tissues was determined by real-time reverse transcriptase polymerase chain reaction.Results Compared with group C-S,the serum BUN and Cr concentrations,renal tubular damage score,and the number of MPO+,F4/80+,and CD3+ cells were significantly increased,and the expression of TNF-α,IL-1β,IL-6 and MIP-2 mRNA was significantly up-regulated in group C-I/R (P＜0.05).Compared with group KO-S,the serum BUN and Cr concentrations,renal tubular damage score,and the number of MPO+,F4/80+,and CD3+ cells were significantly increased,and the expression of TNF-α,IL-1β,IL-6 and MIP-2 mRNA was significantly up-regulated in group KO-I/R (P＜0.05).Compared with group C-I/R,the serum BUN and Cr concentrations,renal tubular damage score,and the number of MPO+,F4/80+,and CD3+ cells were significantly decreased,and the expression of TNF-c,IL-1β,IL-6 and MIP-2 mRNA was significantly down-regulated in group KO-I/R (P＜0.05).Conclusion CXCL16 is involved in the pathophysiological process of renal I/R injury in the mice.
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Objective To evaluate the effects of intrathecal TRESK gene recombinant adenovirus on inflammatory responses mediated by chemokine in the spinal cord of rats with neuropathic pain ( NP ) . Methods Thirty?six male Sprague?Dawley rats, weighing 200-250 g, were randomly divided into 6 groups (n=6 each) using a random number table: control group (group C); sham operation group (group S);NP group; TRESK?overexpressed adenovirus group ( group TRESK ); negative adenovirus group ( group Virus); normal saline group ( group NS) . Spinal nerve injury was produced by exposing the sciatic nerve and its branches and ligation and transection of tibial nerve and common fibular nerve in anesthetized rats. In TRESK, Virus and NS groups, pAd∕CMV∕V5?DEST?TRESK 25 μl (109IU∕ml), negative adenovirus 25 μl and normal saline 25 μl were intrathecally injected, respectively. At 1 day before operation ( base?line, T0 ) and 1, 3, 7 and 14 days after operation ( T1-4 ) , the mechanical paw withdrawal threshold ( MWT) and thermal paw withdrawal latency were measured. Six rats in each group were sacrificed after measurement of pain threshold at T3 . The L4,5 segments of the spinal cords were removed for determination of monocyte chemotactic protein?1 ( MCP?1) , MIP?2, tumor necrosis factor?alpha ( TNF?α) , interleukin?1 beta ( IL?1β) and IL?6 mRNA expression by real?time PCR. Results There was no significant difference in thermal paw withdrawal latency at each time point between groups. Compared with C and S groups, MWT at T1-4 in NP and TRESK groups and at T1-3 in Virus and NS groups were significantly decreased, and the expression of MCP?1, MIP?2, TNF?α, IL?1βand IL?6 mRNA was up?regulated in NP, TRESK, Virus and NS groups. Compared with group NP, MWT was significantly increased at T1-4, and the expres?sion of MCP?1, MIP?2, TNF?α, IL?1β and IL?6 mRNA was down?regulated in group TRESK. Conclusion The mechanism by which intrathecal TRESK gene recombinant adenovirus reduces NP is re?lated to inhibition of inflammatory responses mediated by chemokine in the spinal cord of rats.