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Objective:To evaluate the relationship between chemokine CXC-ligand 16 (CXCL16) and natural killer T cells during renal fibrosis in mice with acute kidney injury (AKI).Methods:Twenty-four healthy male C57BL/6 mice, aged 8-10 weeks, weighing 20-30 g, were divided into 4 groups ( n=6 each) using a random number table method: control group (group C), AKI group, control+ rCXCL16 group (group C-rCXCL16) and AKI+ rCXCL16 group.In AKI-rCXCL16 and AKI groups, folic acid 250 mg/kg was intraperitoneally injected to induce AKI in anesthetized mice, and rCXCL16 0.1 mg/kg and the equal volume of solution were intraperitoneally injected, respectively, at 3, 6, 9 and 12 days after injection of folic acid.The equal volume of solution and rCXCL16 were intraperitoneally injected at the corresponding time points in group C and group C-rCXCL16, respectively.The orbital blood samples were taken on day 14 after injection of folic acid for determination of the serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.The renal tissues were obtained for measurement of the renal fibrosis size (using Sirius red staining and Masson staining), for determination of the expression of fibronectin (FN), collagen-Ⅲ (Col-Ⅲ) and α-smooth muscle actin (α-SMA) (by immunofluorescence) and expression of interleukin-4 (IL-4), mannose receptor (CD206) and arginase 1 (Arg-1) mRNA (by real-time polymerase chain reaction), and for evaluation of the ratio of CD1d Tetramer + -IL-4 + cells (by flow cytometry). Results:Compared with group C, the serum BUN and Cr concentrations were significantly increased, the renal fibrosis size was increased, the expression of IL-4, CD206, Arg-1 mRNA, FN, Col-Ⅲ and α-SMA was up-regulated, and the ratio of CD1d Tetramer + -IL-4 + cells was increased in AKI and AKI-rCXCL16 groups ( P<0.05), and no significant change was found in the parameters mentioned above in group C-rCXCL16 ( P>0.05). Compared with group AKI, the serum BUN and Cr concentrations were significantly increased, the renal fibrosis size was increased, the expression of IL-4, CD206, Arg-1 mRNA, FN, Col-Ⅲ and α-SMA was up-regulated, and the ratio of CD1d Tetramer + -IL-4 + cells was increased in group AKI-rCXCL16 ( P<0.05). Conclusion:The mechanism by which CXCL16 is involved in the process of renal fibrosis is related to the recruitment of natural killer T cells secreting IL-4 which regulates macrophage M2 polarization in mice with AKI.
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Objective To investigate the relationship between clinical parameters related to acute bacterial dysentery and other infectious diarrhea in adults.Methods From April to October 2018,70 patients with clinical diagnosis of acute bacterial dysentery,180 patients with clinical diagnosis of infectious diarrhea and 399 patients with diarrhea to be examined were investigated retrospectively.The collected data included gender,age,time from onset to treatment,maximum body temperature,main symptoms,epidemiological history,blood routine,C-reactive protein and stool routine.Analysis of these clinical factors related to acute bacterial dysentery and other infectious diarrhea.Results A total of 70 patients with acute bacterial dysentery,180 patients with other infectious diarrhea and 399 patients with diarrhea of unknown origin were investigated.The positive rate of epidemiology in the three groups was statistically significant (P ＜0.05);the age of onset of bacterial dysentery was younger than that in patients with diarrhea of unknown orion (P＜O.05).Compared with the other two groups of patients,the onset to visit time was earlier,the number of vomiting was higher,the incidence of fever and tenesmus was higher,and the levels of white blood cells,neutrophils and C-reactive protein were significantly increased (P ＜ 0.05).Conclusions Patients with acute bacterial dysentery,other infectious diarrhea,and diarrhea of unknown origin have some differences in epidemiological history,age at onset,clinical manifestations,and laboratory tests.
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Objective@#To investigate the relationship between clinical parameters related to acute bacterial dysentery and other infectious diarrhea in adults.@*Methods@#From April to October 2018, 70 patients with clinical diagnosis of acute bacterial dysentery, 180 patients with clinical diagnosis of infectious diarrhea and 399 patients with diarrhea to be examined were investigated retrospectively. The collected data included gender, age, time from onset to treatment, maximum body temperature, main symptoms, epidemiological history, blood routine, C-reactive protein and stool routine. Analysis of these clinical factors related to acute bacterial dysentery and other infectious diarrhea.@*Results@#A total of 70 patients with acute bacterial dysentery, 180 patients with other infectious diarrhea and 399 patients with diarrhea of unknown origin were investigated. The positive rate of epidemiology in the three groups was statistically significant (P<0.05); the age of onset of bacterial dysentery was younger than that in patients with diarrhea of unknown origin (P<0.05). Compared with the other two groups of patients, the onset to visit time was earlier, the number of vomiting was higher, the incidence of fever and tenesmus was higher, and the levels of white blood cells, neutrophils and C-reactive protein were significantly increased (P<0.05).@*Conclusions@#Patients with acute bacterial dysentery, other infectious diarrhea, and diarrhea of unknown origin have some differences in epidemiological history, age at onset, clinical manifestations, and laboratory tests.
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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 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 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 observe the effect of acute normovolemic hemodilution(ANH)combined with enhanced recovery after surgery(ERAS)on immune function in patients undergoing hepatic lobectomy. Methods 80 patients were divided into two groups:ERAS group(group E),ANH combined with ERAS group(group AE). bleeding volume,blood transfusion,infused fluid volume,urine output during operation and clinical index after surgery were recorded. Exhaust and defecation time ,fluid intake time and hospitalization duration were also record-ed. Blood samples were obtained from the patients at 30 min before anesthesia induction(T1),immediately(T2), 24 h(T3),3 d(T4)and 7 d(T5)after the end of operation for determination of the expression of CD3+,CD4+, CD8+ on T cells and natural killer cell. Results In group E ,CD3+,CD4+ T-lymphocytes and NK cells at T2-3 decreased as compared with T0. Compared with group E ,no allogeneic blood transfusion cases were found and clinical index duration was shorter in group AE. CD3+,CD4+T-lymphocytes and NK cells at T2-3 increased in group AE as compared with those in Group E. The difference is significant (P < 0.05). Conclusion ANH combined with ERAS can decrease allogenic blood transfusion and increase post-operation immunologic function ,shorten the postoperative hospitalization time.
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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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<p><b>OBJECTIVE</b>To investigate the effect of KN93, a calmodulin-dependent protein kinase II (CaMK II) inhibitor, on SH-SY5Y cell injury induced by bupivacaine hydrochloride.</p><p><b>METHODS</b>SH-SY5Y cells exposed for 24 h to 1 mmol/L KN93, 1 mmol/L bupivacaine hydrochloride, or both were examined for morphological changes and Cav3.1 protein expressions using Western blotting. The vitality and apoptosis rate of the cells at different time points during the exposures were assessed with MTT assay and flow cytometry, respectively.</p><p><b>RESULTS</b>Bupivacaine hydrochloride exposure caused obvious cell morphologial changes, reduced cell viability, increased cell apoptosis, and enhanced Cav3.1 protein expression. All these changes were partly reversed by treatment of the cells with 1 mmol/L KN93.</p><p><b>CONCLUSIONS</b>CaMKII may play a role in bupivacaine hydrochloride-induced SH-SY5Y cells injury, which is related with upregulated Cav3.1 protein expression.</p>
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Humans , Apoptosis , Bupivacaine , Calcium Channels, T-Type , Metabolism , Calcium-Calmodulin-Dependent Protein Kinase Type 2 , Metabolism , Cell Line , Cell Survival , Up-RegulationABSTRACT
Objective To evaluate the effects of sufentanil and morphine on cisplatin-induced acute kidney injury in rats.Methods Thirty-two healthy Sprague-Dawley rats, aged 8-10 weeks, weighing 220-280 g, were randomly divided into 4 groups (n =8 each) using a random number table: control group (group C);cisplatin group (group Cis);sufentanil group (group S);morphine group (group M).Cisplatin 16 mg/kg was injected intraperitoneally in group Cis.In group S, cisplatin 16 mg/kg was injected intraperitoneally, followed by injection of sufentanil 2 μg/kg over 5 min via the caudal vein for 3 consecutive days.In group M, cisplatin 16 mg/kg was injected intraperitoneally, followed by injection of morphine 2 μg/kg over 5 min via the caudal vein for 3 consecutive days.The equal volume of normal saline was given in group C.After the end of administration on 3rd day, blood samples were collected from the orbital venous plexus for measurement of serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.The animals were then sacrificed, and the left kidney specimens were obtained for examination of the pathological changes (under the light microscope) and for determination of the tumor necrosis factor-alpha (TNF-α) , interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) concentrations (by enzyme-linked immunosorbent assay) , and expression of X-linked inhibitor of apoptosis protein (XIAP) , suvivin and caspase-3 (by Western blot).Periodic acid-Schiff's staining was used to evaluate the pathological changes of the renal tubule.Results Compared with group C, the serum BUN, Cr concentrations and renal tubule injury score were significantly increased, the contents of TNF-α, IL-1β and IL-6 were increased, the expression of XIAP and suvivin was down-regulated, and the expression of caspase-3 was up-regulated in Cis,S and M groups (P＜0.05).Compared with group Cis, the serum BUN and Cr concentrations and renal tubule injury score were significantly decreased, the contents of TNF-α, IL-1β and IL-6 were decreased, the expression of XIAP and suvivin was up-regulated, and the expression of caspase-3 was down-regulated in S and M groups (P＜0.05).There were no significant differences in the indexes mentioned above between group S and group M (P＞0.05).Conclusion Both sufentanil and morphine can reduce cisplatin-induced acute kidney injury in rats with similar efficacy, and the mechanism may be related to the inhibition of the inflammatory responses and cell apoptosis.
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Objective To evaluate the effects of sevoflurane on invasion and migration of mouse lung cancer cells induced by hypoxia.Methods Mouse Lewis lung cancer cells were inoculated in the culture plate.After being cultured for 24 h,the cells were randomly divided into 3 groups (n=18 each) using a random number table:control group (group C),hypoxia group (group H) and hypoxia+ 2％ sevoflurane group (group HS).Cells were exposed to 95％ air-5％CO2 (2 L/min) for 4 h in group C.Cells were exposed to 94％ N2-5％CO2-1％ O2 for 4 h in group H.In group HS,cells were exposed to 2％ sevoflurane and 94％ N2 (2 L/min) for 4 h.The invasion of cells was determined by Transwell assay,and the invaded cells were counted.The migration of cells was evaluated by wound healing assay,and cell migration rates were calculated.The expression of Beclin 1 and LC3 Ⅱ protein in cells was detected by Western blot.Results Compared with group C,the number of invaded cells and cell migration rates were significantly increased,and the expression of Beclin Ⅰ and LC3 Ⅱ was up-regulated in H and HS groups.Compared with group H,the number of invaded cells and cell migration rates were significantly decreased,and the expression of Beclin 1 and LC3 Ⅱ was down-regulated in group HS.Conclusion Sevoflurane can inhibit the invasion and migration of mouse lung cancer cells induced by hypoxia,and inhibition of autophagy is involved in the mechanism.
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Objective To preliminarily evaluate the role of Ras homolog gene (Rho)/Rho-associated coiled coil-forming protein kinase (ROCK) signaling pathway in propofol-induced inhibition of metastasis of human gastric cancer cells.Methods Human gastric cancer MKN-45 cells cultured in vitro,with the concentration of 1.0× 106 cells/ml,were seeded in culture plates,and incubated for 24 h.The plates were then randomly divided into 4 groups using a random number table:control group (group C),propofol group (group P),lysophosphatidic acid group (group L) and propofol + lysophosphatidic acid group (group PL).Group C received no administration.In group P,propofol at the final concentration of 16 μg/ml was given.In group L,lysophosphatidic acid at the final concentration of 1 μmol/L was administered.In group PL,propofol and lysophosphatidic acid were given with the final concentration of 16 μg/ml and 1 μmol/L,respectively.All the cells were then incubated for another 24 h.The migration of cells was determined by wound healing assay,and cell migration rates were calculated.The invasion of cells was determined by Transwell assay,and the invaded cells were counted.The expression of matrix metalloproteinases-2 (MMP-2),MMP-9,RhoA,and ROCK1 in cells was detected by Western blot.Results Compared with group C,cell migration rates and the number of invaded cells were significantly increased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was up-regulated in group L,and cell migration rates and the number of invaded cells were decreased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was down-regulated in group P.Compared with group L,cell migration rates and the number of invaded cells were significantly decreased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was down-regulated in group PL.Conclusion Inhibition of RhoA/ROCK1 signaling pathway is involved in the mechanism by which propofol decreases metastasis of human gastric cancer cells.
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Objective To evaluate the effect of propofol on invasiveness of human gastric cancer MKN-45 cells.Methods Human gastric cancer cell line MKN-45 were seeded in culture plates.After being cultured for 24 h,the cells were randomly divided into 5 groups(n =12 each):control group (group C),intralipid group (group Ⅰ),4 μg/ml propofol group (group P1),8 μg/ml propofol group (group P2) and 16μg/ml propofol group (group P3).The cells were treated with 10％ intralipid and 4,8 and 16 μg/ml propofol for 24 h in I and P1-3 groups,respectively.The cells were then cultured for another 24 h.The migration of cells was determined by cell scratch test.The invasion of cells was determined by Transwell invasion assay.The expression of RhoA and ROCK1 was detected by Western blot.Results Compared with group C,the cell migration and invasion were significantly decreased,and the expression of RhoA and ROCK1 was down-regulated in P1-3 groups,and no significant changes were found in the parameters mentioned above in group Ⅰ.With the increasing concentrations of propofol,the cell migration and invasion were gradually decreased,and the expression of RhoA and ROCK1 was gradually down-regulated in P1-3 groups.Conclusion Propofol can inhibit the invasiveness of human gastric cancer MKN-45 cells cultured in vitro dose-dependently and inhibition of RhoA/ROCK1 signaling pathway may be involved in the mechanism.
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Objective To investigate the effects of sevoflurane on inhibition of growth of human lung adenocarcinoma A549 cells by cisplatin and γ ray.Methods The human lung adenocarcinoma cell line A549 was seeded in culture plate.After being cultured for 24 h,the cells were randomly divided into 6 groups (n =6each):control group (group C),sevoflurane group (group S),cisplatin group (group D),cisplatin + sevoflurane group (group DS),γ ray group (group R) and γ ray + sevoflurane group (group RS).A549 cells were exposed to 2.5% sevoflurane for 4 h in group S.Cisplatin with the final concentration of 3 mg/L was added to the culture medium and the cells were then incubated for 4 h in group D.Cisplatin with the final concentration of 3 mg/L was added to the culture medium and the cells were then exposed to 2.5 % sevoflurane for 4 h in group DS.A549 cells were exposed to γ irradiation (2 Gy) for 4 h in group R.A549 cells were exposed to γ irradiation (2Gy) and to 2.5% sevoflurane for 4 h in group RS.The cells were cultured for another 24 h after the end of treatment,the colony formation was detected and the rate of colony formation was calculated by colony formation assay.Proliferation of A549 cells was measured by plate colony formation and MTF assay and the rate of proliferation inhibition was calculated.Cell apoptosis was detected with flow cytometer.The expression of X-linked inhibitor of apoptosis protein (XIAP) and caspase-3 was detected by Western blot.Results Compared with group C,the rate of colony formation was significantly decreased,the rate of proliferation inhibition and percentage of apoptotic cells were increased,XIAP expression was down-regulated and caspase-3 expression was up-regulated in groups S,D,DS,R and RS (P ＜ 0.05).The rate of colony formation was significantly lower,the rate of proliferation inhibition and percentage of apoptotic cells were higher,XIAP expression was lower and caspase-3 expression was higher in group DS than in groups S and D,and in group RS than in groups S and R (P ＜ 0.05).Conclusion Sevoflurane can enhance cisplatin and γ ray-induced inhibition of growth of human lung adenocarcinoma A549 cells,and downregulation of XIAP expression and up-regulation of caspase-3 expression may be involved in the mechanism.
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Objective To investigate the effect of propofol on the invasion of human liver cancer cell line HepG2.Methods HepG2 cell were seeded in 96-well plates (100μl/hole) with a density of 1 × 105/ml and randomly divided into 5 groups (n =9 each):control group (group C),intralipid group (group Ⅰ),and propofol 30,60 and 120 μg/ml groups (groups P1-3).Propofol 30,60 and 120 μg/ml were added to the culture medium in groups P1-3,respectively,and then the cells were cultured for 48 h.In group Ⅰ,10％ intralipid was added to the culture medium and then the cells were cultured for 48 h.The invasion of cells was measured by Transwell invasion assay at 48 h of incubation.The expression of matrix metalloproteinases-2 (MMP-2) and mRNA and matrix metalloproteinases-9 (MMP-9) and mRNA was determined at 48 h of incubation.Results Compared with group C,the invasion of HepG2 cells was significantly decreased and the expression of MMP-2,MMP-9 and MMP-2 mRNA and MMP-9 mRNA was down-regulated in groups P1-3 (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group Ⅰ (P ＞ 0.05).The invasion of HepG2 cells was gradually decreased and the expression of MMP-2,MMP-9 and MMP-2 mRNA and MMP-9 mRNA was gradually down-regulated in groups P1-3 (P ＜0.05).Conclusion Propofol can inhibit the invasion of HepG2 cells in a concentration-dependent manner and down-regulation of the expression of MMP-2 and MMP-9 may be involved in the mechanism.
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Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) in the up-regulation of expression of Cav3.2 T-type calcium channels in spinal cord in a rat model of neuropathic pain (NP).Methods Forty-eight male Sprague-Dawley rats,aged 3 months,weighing 220-250 g,were randomly divided into 6 groups (n =8 each)∶ sham operation group (group S),group NP,dimethyl sulfoxide group (group D) and different concentrations of a specific CaMK Ⅱ inhibitor KN93 groups (groups K1-3).NP was produced by chronic compression of dorsal root ganglion.The rats in groups D and K1-3 received a single intrathecal injection of dimethyl sulfoxide and KN93 15,30,60 nmol/L (10 μl),respectively,on 5th day after NP.Paw withdrawal threshold to von Frey filament stimulation (MWT) and paw withdrawal latency to thermal nociceptive stimulus (TWL) were measured before NP,before intrathecal injection on 5th day after NP,and at 30 and 60 min and 3,6 and 8 h after intrathecal injection on 5th day after NP (T1-7).The rats were sacrificed after the measurement of pain threshold at T7 and their lumbar enlargements were removed to detect the expression of Cav3.2 mRNA and protein using Western blot and RT-PCR.Results Compared with group S,MWT was significantly decreased,TWL was shortened and the expression of Cav3.2 mRNA and protein was up-regulated in NP,D and K1-3 groups (P ＜ 0.05).Compared with NP group,MWT was significantly increased,TWL was prolonged and the expression of Cav3.2 mRNA and protein was down-regulated in a concentration-dependent manner in K1-3 groups (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group D (P ＞ 0.05).Conclusion CaMK Ⅱ is involved in the development and maintenance of chronic NP by up-regulating the expression of Cav3.2 T-type calcium channels in rat spinal cord.
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Objective To evaluate the effect of propofol on proliferation of human liver cancer cell line HepG2.Methods HepG2 cells were seeded in 96-well plates (100μl/hole) with a density of 1 × 105/ml and randomly divided into 5 groups (n =33 each)∶ control group (group C),group intralipid (group Ⅰ),and propofol 30,60 and 120μg/ml groups (groups P1-3).In groups P1-3,propofol 30,60 and 120 μg/ml were added to the culture medium and then the cells were cultured for 72 h.In group Ⅰ,10％ intralipid was added to the culture medium and then the cells were cultured for 72 h.The morphology of cells was observed with the light microscope after 24 h of incubation with propofol.The proliferation of the cells was determined at 0,24,48 and 72 h of incubation with propofol.The expression of Fas was determined at 48 h of incubation with propofol.Results The number of the cells was gradually smaller in groups P1-3.The proliferation of the cells was significantly higher in group Ⅰ,while lower in groups P1-3 than in group C (P ＜ 0.05).There was no significant difference in the expression of Fas between group Ⅰ and group C (P ＞ 0.05).The expression of Fas was significantly higher in groups P1-3 than in group C (P ＜ 0.05).The proliferation of the cells was significantly lower,and the expression of Fas was significantly higher in group P3 than in group P1 or group P2 (P ＜ 0.05).Conclusion Propofol can inhibit the proliferation of human liver cancer cell line HepG2 in a concentration-dependent manner and up-regulation of the expression of Fas is involved in the mechanism.