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Objective:To investigate the effect of autophagy on liver injury with obstructive jaundice in Sprague-Dawley (SD) rats and its underlying mechanism.Methods:Thirty-five healthy male SD rats, SPF grade, aged 6-8 weeks, weighting 200-300 g, were divided into 5 groups with 7 rats in each group, including sham group (simple free common bile duct, without ligation, intraperitoneal injection of normal saline), obstructive jaundice (OJ) group (established by common bile duct ligation, intraperitoneal injection of normal saline), OJ group with 3-MA, OJ group with Rapamycin, and OJ group with 3-MA and VX-765. Morphological changes in liver tissues were analyzed with HE staining. Expression of autophagy-related protein Atg5 was detected by immunohistochemistry staining. Liver function was analyzed by automatic biochemical instrument and the level of serum interleukin (IL)-18 was detected using ELISA assay. Protein levels of autophagy related-proteins and endoplasmic reticulum stressed (ERs)-related apoptosis proteins were detected by Western Blot.Results:The relative expression of autophagy related protein Atg5 in OJ group was significantly higher than that in sham group [(5.0±1.0) vs. (2.8±1.3), t=-3.00, P<0.05]. Compared with sham group, the activity of autophagy was enhanced and the protein levels of Caspase-1/p-65 and IL-18 were significantly increased in OJ group. At the same time, apoptosis was induced by activating ERs. In OJ group, the autophagy inducer 3-MA improved the expression levels of Caspase-1/p-65 and IL-18, and aggravate liver injury. While after applying the autophagy agonist Rapamycin in OJ rat models, the expression of Caspase-1/p-65 and IL-18 was repressed and liver damage was also reduced. In addition, in rat OJ groups with 3-MA, inhibition of Caspase-1 by VX-765 could down regulate the expression of Caspase-1/p-65 and IL-18, and protect against liver injury. Conclusions:Both ERs related apoptosis and autophagy were activated after ligation of common bile duct. Besides, activation of autophagy could reduce OJ-induced liver injury in SD rats by inhibiting the Caspase-1/p-65 inflammatory pathway.
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Objective:To investigate the effect of cell migration-inducing hyaluronidase 1 (CEMIP) on biological function of gallbladder cancer GBC-SD cells and its possible mechanism.Methods:The expression of CEMIP in biliary epithelial cell line HIBEC and gallbladder cancer cell line NOZ and GBC-SD was detected by Western blot. GBC-SD cells in logarithmic growth phase were divided into blank control group, negative control group (transfection with nonsense siRNA), siCEMIP-1 group (transfection with siCEMIP-1) and siCEMIP-2 group (transfection with siCEMIP-2). The expression of CEMIP and binding immunoglobulin protein (Bip) and calreticulin (CRT) in GBC-SD cells was detected by Western blot after culturing for 48h in blank control group, negative control group, siCEMIP-1 and siCEMIP-2 group. The relative survival rate was determined by CCK-8 assay. The wound healing rate and apoptotic rate was detected by wound healing assay and flow cytometry. The migration and invasion abilities were evaluated by Transwell chamber assay. Twelve 5-week-old BALB/c-nude mice were selected and divided into control group and experimental group (6 mice in each group). GBC-SD cells and GBC-SD cells with silenced CEMIP were subcutaneously injected into the right armpit (forelimb) of the two groups of mice, respectively. The volume and weight of transplanted tumor were compared 33 days later.Results:Compared with HIBEC cells, the relative protein level of CEMIP in gallbladder cancer GBC-SD cells [(0.750±0.034) vs. (0.120±0.002)] and NOZ cells [(0.690±0.013) vs. (0.120±0.002)] was significantly higher ( P<0.05). Compared with blank control group and negative control group, the relative protein level of CEMIP, Bip and CRT in siCEMIP-1 group and siCEMIP-2 group was significantly lower ( P<0.05). Compared with blank control group and negative control group, the relative survival rate and wound healing rate and number of migration cells and invading cells in siCEMIP-1 group and siCEMIP-2 group were also significantly lower ( P<0.05). While the apoptotic rate in siCEMIP-1 group and siCEMIP-2 group were higher than that in blank control group and negative control group ( P<0.05). Compared with control group, the average tumor volume [(543.6±114.7) vs. (801.5±256.3) mm 3] and tumor weight [(0.453±0.093) vs. (0.728±0.278) g ] of the experimental group was significantly decreased ( P<0.05). Conclusions:CEMIP was up-regulated in gallbladder cancer cell line GBC-SD and NOZ. Silencing CEMIP inhibited cell proliferation, wound healing rate, migration and invasion, and promoted apoptosis in gallbladder cancer GBC-SD cells, which may be related to the inhibition of endoplasmic reticulum chaperone Bip and CRT expression.
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【Objective】 To investigate the expression of pyruvate kinase M2 (PKM2) in intrahepatic cholangiocarcinoma (ICC) and the effect of PKM2 on the proliferation and epithelial-to-mesenchymal transition (EMT) of ICC cells. 【Methods】 PKM2 expression was evaluated in ICC tissues and cell lines by Real-time quantitative reverse-transcription polymerase chain reaction (RT-PCR), and immunohistochemistry assays. In vitro, we knocked down PKM2 expression in ICC cell lines and investigated the biological function and the underlying mechanism of PKM2 in ICC. 【Results】 RT-PCR results showed that PKM2 was highly expressed in ICC (P<0.05). Moreover, PKM2 knockdown inhibited cell proliferation and the invasive capacities of ICC cells, and inhibited Wnt/ β-Catenin signaling, which subsequently regulated EMT signaling pathway in vitro. 【Conclusion】 PKM2 expression in cholangiocarcinoma is significantly higher than that in adjacent tissues. PKM2 can regulate EMT and invasion and metastasis of ICC via the Wnt/β-Catenin signal.
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Hepatocellular carcinoma (HCC) with bile duct tumor thrombus (BDTT) is rare and enhanced CT or MRI can be used for its diagnosis. Surgical procedure is the main treatment for HCC with BDTT. The authors introduce the experiences of recurrent patient with HCC and BDTT who was treated with targeted therapy plus immunotherapy, in order to provide reference for its clinical diagnosis and treatment.
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Objective@#To explore the effect of aspirin combined with metformin on the apoptosis of thyroid cancer TPC-1 cells and its mechanism.@*Methods@#The proliferation and apoptosis of TPC-1 cells treated with different concentrations of aspirin and metformin were detected using cell count kit-8 (CCK-8) assay and flow cytometry, respectively. Western blot was used to detect the expressions of microtubule-associated protein light chain 3 (LC3), p62 and cysteinyl aspartate specific proteinase 3 (caspase-3) after treatment with aspirin, metformin and 3-Methyladenine (3-MA).@*Results@#The relative cell viability of TPC-1 cells treated with 0.5, 1.0, 2.0, 4.0 mmol/L aspirin for 24 and 48 hours were (85.6±9.1)%, (79.9±8.6)%, (57.0±5.3)%, (55.7±5.4)%; (76.7±2.8)%, (75.4±6.1)%, (46.1±4.1)%, (36.3±3.2)%, respectively. The value of half maximal inhibitory concentration (IC50) for 24 and 48 hours were 4.297 mmol/L, 2.133 mmol/L, respectively. The apoptotic rate in the 1 mmol/L aspirin treatment group and negative control group were (29.2±8.5)%, (4.2±2.9)%, respectively (P<0.05). Moreover, treatment with metformin increased the protein expression of LC3Ⅱ/Ⅰ ratio, and decreased the expression of p62, while treatment with aspirin decreased the expression of LC3Ⅱ/Ⅰ ratio and increased the expression of p62. The relative cell viability of TPC-1 cells treated with metformin, 3-MA, an autophagy inhibitor, and 3-MA combined with metformin were (73.2±9.2)%, (95.8±3.3)%, (59.9±9.2)%, respectively. The apoptotic rates in these groups were (35.5±1.5)%, (12.3±1.4)%, (49.9±5.4)%, respectively. Compared with the metformin group, the relative cell viability in metformin combined with 3-MA group was significantly lower while the apoptotic rate was higher (P<0.05), which indicated that treatment with 3-MA enhanced the metformin-induced apoptosis of TPC-1 cells. The relative cell viability of TPC-1 cells in metformin group, aspirin group, metformin combined with aspirin group were (87.3±11.8)%, (85.7±9.6)%, (72.4±8.8)%, respectively. The apoptotic rates in these groups were (29.7±4.0)%, (30.5±6.5)%, (52.5±4.6)%, respectively. Compared with the metformin or aspirin group, the relative cell viability in metformin combined with aspirin group was significantly lower, while the apoptotic rate was higher (P<0.05), which indicated that aspirin enhanced the metformin-induced apoptosis of TPC-1 cells.@*Conclusions@#Our findings indicate that metformin-mediated autophagy plays a protective role in metformin-induced apoptosis and proliferation inhibition. Aspirin enhances the metformin-induced apoptosis of thyroid cancer TPC-1 cells through inhibition of autophagy.
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Objective@#To explore the clinical efficacy of S-1 single agent adjuvant chemotherapy for the patients undergoing radical resection of extrahepatic biliary carcinoma.@*Methods@#The clinical data of 108 patients with extrahepatic biliary carcinoma receiving radical resection who were admitted from January 2014 to June 2017 were retrospectively analyzed. There were 62 males(57.4%)and 46 females(42.6%),with a median age of 59 years (range:26 to 79 years),10 cases(9.3%) in stage Ⅱ,85 cases(78.7%) in stage Ⅲ, and 13 cases (12.0%) in stage Ⅳ, 40 cases(37.0%) of hilar cholangiocarcinoma, 8 cases(7.4%) of middle cholangiocarcinoma, 25 cases (23.2%) of distal cholangiocarcinoma, 35 cases(32.4%) of gallbladder carcinoma.After radical resection of extrahepatic biliary carcinoma, 49 patients receiving S-1 single agent chemotherapy and 59 patients receiving non-special treatment were divided into the chemotherapy group and the operation group,respectively. All the dates of the patients were followed up and collected with the overall survival time,tumor-free survival time,1,2 and 3-year survival rate after operation,and the rate of major toxic reaction during chemotherapy of the chemotherapy group. Survival curve was drawn by the Kaplan-Meier method, and survival analysis was done using the Log-rank test.@*Results@#There were no significant differences in the general date of two groups(sex, age, tumor size, tumor site, TNM stages, degree of differentiation). The median overall survival time and the median tumor-free survival time in the chemotherapy group were 27 months and 21 months,respectively,and in the operation group were 21 months and 17 months,respectively. There were differences between the two groups in the overall survival rates(χ2=3.967,P<0.05) and the 2 and 3-year survival rate(63.3%,36.6%;41.6%,20.4%;χ2=4.510,P<0.05;χ2=6.143,P<0.05),but the 1-year overall survival rate (83.4%,79.7%)was not statistically significant(χ2=0.286,P>0.05). There were no significant differences in the tumor-free survival time,1,2 and 3-year tumor-free survival rate(77.6%,41.4%,33.1%;62.7%,30.9%,21.2%)between the two groups(χ2=0.876,P>0.05;χ2=0.252,P>0.05;χ2=1.571,P>0.05;χ2=3.323,P>0.05,respectively). The main toxic reaction during chemotherapy were dyspepsia(28.6%, 14/49), anemia(26.5%, 13/49), and leukopenia(22.5%, 11/49), all of which were mild.@*Conclusion@#S-1 single agent chemotherapy after radical reseetion of extrahepatic biliary carcinoma could effectly improve the survival of patients and all of the main toxic reaction during chemotherapy were mild.
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Objective To explore the expression of calreticulin (CRT) in gallbladder cancer tissue and its effect on the biological behavior in gallbladder cancer GBC-SD cells.Methods Immunohistochemistry and RT-qPCR were applied to detect the expression of CRT.Small interfering RNA was transfected into gallbladder cancer GBC-SD cells and Western blotting were used to detect the expression of CRT.The proliferation was determined by using cell counting kit-8 (CCK-8) and clone assays.Flow cytometry were applied to detect the apoptosis and cell cycle.Migration was detected by wound healing and transwell assays,respectively.The expression of p-Akt and MMP-9 were detected by using Western blotting.Results Expression of CRT in gallbladder cancer tissues is higher than adjacent cancer tissues and chronic cholecystitis tissues(t =5.571,P ＜ 0.05).The relative growth rate in the siCRT-1,siCRT-2 experimental group for 24 hours,48 hourrs were 71.5％ ±6.3％,79.5％ ±2.7％;62.6％ ± 8.8％,55.6％ ±2.6％,respectively.The apoptosis rate in the blank group,the negative control group,siCRT-1 and siCRT-2 group were 3.0％ ± 1.8％,4.7％ ± 1.3％,13.6％ ± 1.0％,20.0％ ± 4.0％,respectively.Wound healing assays showed that the wound closure ratio in the blank group,negative control group,siCRT-1 and siCRT-2 group were(0.67 ±0.02),(0.58 ±0.02),(0.22 ±0.01),(0.37 ±0.04),respectively.Transwell experiments showed that the numbers of migration of GBC-SD cells in the blank group,negative control group,siCRT-1 and siCRT-2 group were (302 ± 11),(297 ± 15),(178 ± 10),(165 ± 12),respectively,compared with the blank group and the negative control group,the relative growth rate for 24 hours and 48 hours was significantly lower,the apoptosis rate was higher,the numbers of migration was lower (F =29.310,118.618,69.651,144.515,190.145,P ＜ 0.05).Compared with the blank group and the negative control group,the expression of p-Akt and MMP-9 decreased after down-regulating the expression of CRT.Conclusions The expression of CRT in gallbladder cancer tissue was higher.CRT downregulation mediated changes of biological behaviors in gallbladder cancer may be associated with p-Akt/MMP-9 signal pathway.
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Objective To explore the effect of metformin on the apoptosis of thyroid cancer TPC-1 cells and its mechanism.Methods The proliferation and apoptosis of TPC-1 cells treated with different concentrations of metformin were detected using cell count kit-8(CCK-8)assay and flow cytometry respectively.Western blot and Real-time PCR were used to detect the expression of endoplasmic reticulum chaperone immunoglobulin heavy chain binding protein(Bip)and endoplasmic reticulum stress associated apoptosis protein CCAAT/enhancer-binding protein homologous protein(CHOP)and cysteinyl aspartate specific proteinase(Caspase-12)on mRNA and protein levels.TPC-1 cells were injected into nude mice to investigate the effect of metformin on the tumorigenesis in vivo.In addition,the expressions of Bip and CHOP were detected by an immunohistochemical method.Results Metformin could decrease proliferation and promote apoptosis of TPC-1 cells.Moreover,metformin increased the expression of Bip and endoplasmic reticulum stress-associated apoptosis protein Caspase-12 and CHOP,both in protein and mRNA levels.4-phenylbutyrate,the endoplasmic reticulum stress inhibitor,could reverse the metformin-induced apoptosis of TPC-1 cells.By contrast,activating endoplasmic reticulum stress by thapsigargin enhanced the metformin-mediated apoptosis.The average tumor weight and size in metformin group was significantly lower than that in the control group.Meanwhile,the metformin group had higher expression of Bip and CHOP.Conclusion Metformin may induce the apoptosis of thyroid cancer TPC-1 cells through endoplasmic reticulum stress activation.
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Objective@#To investigate the effects of Kindlin-2 on malignant phenotypes of human gallbladder cancer cells and discuss the mechanisms.@*Methods@#The expression level of Kindlin-2 in 30 cases of gallbladder cancer tissues and adjacent non-tumoral tissues collected from the First Affiliated Hospital of Zhengzhou University between September 2012 and May 2013 was assessed by real-time PCR and immunohistochemistry.Lentivirus-mediated Kindlin-2 overexpression was used in gallbladder cancer cell lines GBC-SD and SGC-996.Transwell assay and adhesion assay were investigated to explore the functional role of Kindlin-2 on gallbladder cancer cells.Western Blot was used to test the protein change of epithelial-mesenchymal transition(EMT) characteristics. The t-test was used to analyzed results.@*Results@#The RNA and protein levels of Kindlin-2 in gallbladder cancer tissues were higher than in the non-tumoral tissues (t=4.372, P=0.001; t=7.477, P=0.000). The expression level of Kindlin-2 in gallbladder cancer tissues was correlated with Nevin stage(χ2=5.932, P=0.035). Compared with control groups, the cell-matrix adhesion ability of GBC-SD and SGC-996 with Kindlin-2 overexpression was obviously promoted(1.66±0.03 vs. 1.07±0.22, t=2.710, P=0.041; 2.66±0.24 vs. 1.03±0.02, t=6.610, P=0.020). The number of GBC-SD and SGC-996 cells with Kindlin-2 overexpression passing through the Transwell chamber matrix increased significantly compared with the control groups(116.1±13.9 vs. 54.7±8.4, t=3.781, P=0.019; 136.3±7.5 vs. 64.3±6.4, t=7.302, P=0.002). The wound healing rate of GBC-SD with Kindlin-2 overexpression at 12-hour and 24-hour was higher than that of the group ((42.9±2.2)% vs. (29.7±1.7)%, t=4.690, P=0.009; (65.0±2.4)% vs.(40.4±2.0)%, t=7.945, P=0.001). The wound healing rate of SGC-996 with Kindlin-2 overexpression at 12-hour and 24-hour was also higher than that of the group ((32.9±1.3)% vs. (24.1±1.5)%, t=4.518, P=0.011; (51.3±1.1)% vs. (39.2±1.1)%, t=8.001, P=0.001). The characteristics of EMT were induced in gallbladder cancer cells with Kindlin-2 overexpression, including the up-regulation of N-cadherin, Vemintin and the down-regulation of E-cadherin.@*Conclusion@#The expression of Kindlin-2 is up-regulated in gallbladder cancer tissues and Kindlin-2 promoted the malignant phenotypes of gallbladder cancer cells partially by epithelial-mesenchymal transition.
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Objective To study the expression and the clinical significance of hypoxia-induced factor-1α (HIF-1α) in gallbladder cancer tissues,and the role and mechanism of HIF-1α in metformin-suppressed metastasis in gallbladder carcinoma GBC-SD cells.Methods 24 specimens of gallbladder cancer tissues and 5 specimens of chronic cholecystitis were collected from the First Affiliated Hospital of Zhengzhou University between June 2016 and February 2017.Immunohistochemistry and qPCR were used to detect the expression of HIF-1α in gallbladder cancer tissues,in adjacent non-cancer tissues and in chronic cholecystitis,and the clinical significance was analyzed.The model of metastasis was induced by hypoxia;the wound healing assay and the Transwell assay were used to detect the ability of cell metastasis;the expressions of HIF-1α and VEGF in gallbladder carcinoma GBC-SD cells were detected by western blotting assay and immunofiuorescence.Results The expression of HIF-1α in gallbladder cancer tissues was higher than the adjacent non-cancer tissues and in chronic cholecystitis.The expression of HIF-1α was correlated with lymph node metastasis and TNM staging in gallbladder cancer tissues (P ＜ 0.05).The wound healing rate after 48 h in the negative control group and in the treatment with hypoxia group (1％ O2) in GBC-SD cells were (46.5 ± 4.8) ％ and (67.3 ± 4.0) ％,respectively.The Transwell data showed that the numbers of metastasis after 24 h in the negative control group and in the treatment with hypoxia group GBC-SD cells were (147.4 ± 11.7) and (234.4 ± 17.7),respectively.When compared with the negative control group,treatment with hypoxia significantly increased the ability of metastasis and up-regulated the expression of HIF-1α and VEGF in GBC-SD cells (P ＜ 0.05).The wound healing rate after 48 h in the negative control group,the metformin group,the hypoxia group and the metformin and hypoxia group in GBC-SD cells were (40.6 ± 7.1) ％,(16.4 ± 9.4) ％,(69.5 ± 4.0) ％ and (22.4 ± 7.4) ％,respectively.The Transwell data showed that the numbers of metastasis after 24 h in the negative control group,the metformin group,the hypoxia group and the metformin and hypoxia group in GBC-SD cells were (148.4 ± 6.9),(90.0 ± 8.4),(185.8 ± 10.2) and (113.4± 8.6),respectively.When comparcd with the hypoxia group,treatment with metformin and hypoxia significantly decreased the ability of metastasis and down-regulated the expression of HIF-1α and VEGF in GBC-SD cells (P ＜ 0.05).The wound healing rate after 48 h in the negative control group,the 2MeoE2 group,the hypoxia group,the 2MeoE2 and hypoxia group in GBC-SD cells were (43.4 ±4.4)％,(25.9 ±9.0)％,(63.3 ±2.2)％,(46.2 ±4.5)％,respectively.The Transwell data showed that the numbers of metastasis after 24 h in the negative control group,the 2MeoE2 group,the hypoxia group,the 2MeoE2 and hypoxia group in GBC-SD cells were (144.2 ± 12.6),(80.2 ±7.7),(203.8 ±7.0),(124.0 ± 5.2),respectively.When compared with the hypoxia group,treatment with HIF-1α inhibitor 2MeoE2 and hypoxia significantly decreased the ability of metastasis and down-regulated the expression of HIF-1α and VEGF in GBC-SD cells (P ＜ 0.05).Conclusions The expression of HIF-1 α was correlated with lymph node metastasis and TNM staging in gallbladder cancer tissues.Treatment with hypoxia significantly increased the expression of HIF-1α and VEGF and promoted metastasis of GBC-SD cells,while treatment with metformin decreased the ability of metastasis induced by hypoxia via inhibiting the HIF-1o/VEGF pathway in GBC-SD cells.
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As a nuclear transcription repressor,the functions of TGIF are complicated,not only represses target genes expression directly,but also takes part in the regulation of multiple important cellular signaling pathways,which are associated with the differentiation of cells and tissues,inflammation,metabolism and tumors.In past few years,more and more studies on the role of TGIF in tumors suggest TGIF may be a new therapy target in the diagnosis and treatment of tumours.This article mainly reviews the research progress of TGIF in some signaling pathways like TGF-β,MAPK,PI3K/AKT,and tumours like hepatocellular carcinoma,lung carcinoma and urinary tract urothelial carcinoma.
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Pancreatic tuberculosis (PTB) is a rare,chronic,specific and infectious disease which is generally secondary to tuberculosis at the common sites of pancreas,and it has a high misdiagnosis rate due to the hidden onset and nonspecific symptoms of PTB.A patient with PTB was admitted to the First Affiliated Hospital of Zhengzhou University in June 2014.Before operation,the space-occupying lesions of the head of pancreas were detected by preoperative imaging examination,and the patient was regarded as with pancreatic cancer.Intraoperative exploration showed cystic duct involvement,and the granulomatous inflammation was detected by rapid pathological examination using frozen section technique,after that the patient received granuloma resection+cholecystectomy according to suspected PTB.The diagnosis of PTB was confirmed by postoperative pathological examination,and the patient received liver-protective and anti-tuberculosis treatments after discharge.
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Objective To explore the effect of calreticulin (CRT) on cell proliferation and invasion of human hepatocellular carcinoma cell line SMMC-7721 and HepG2.Methods SMMC-7721 and HepG2 cells were transfected with small interfering RNA (siRNA).The transfection rate was detected by immunoflurescence and western blot.The cell proliferation,invasion and apoptosis of SMMC-7721 and HepG2 cells were determined by using cell counting kit-8 (CCK-8) assays,transwell assays and flow cytometry,respectively.The p-Akt and Akt levels were detected by western blot.Results The growth inhibition rate in the siRNA experimental group of SMMC-7721 and HepG2 cells for 24,36 and 48 h were (41.0 ±2.2) ％,(46.5 ±1.6)％,(59.7 ±2.2)％ and (36.8 ±2.7)％,(47.3 ± 1.8)％,(61.5 ±3.2)％,respectively.The apoptosis rate after down-regulating the expression of CRT in SMMC-7721 and HepG2 cells for 36h were (45.2 ± 9.1) ％ and (48.9 ± 8.0) ％,respectively.Compared with the blank group and the negative control group,the growth inhibition rate in the siRNA experimental group was lower (P ＜0.05),but the apoptosis rate was significantly higher (P ＜ 0.05).Transwell experiments confirmed that the numbers of invaded SMMC-7721 and HepG2 cells in the blank group and the negative control group and siRNA experimental group were (96.8±7.3),(95.6±5.4),(34.0±4.2) and (124.0 ±9.9),(121.6 ±7.0),(70.4±9.5),respectively,indicating that cell invasion in the siRNA experimental group was significantly suppressed (P ＜ 0.05).The expression of p-Akt was decreased (P ＜ 0.05) after down-regulating the expression of CRT for 36h.Conclusion CRT gene silencing by siRNA can inhibit the SMMC-7721 and HepG2 cell proliferation and invasion,but increase the cell apoptosis by regulating PI3K/Akt signal pathway.
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Objective To assess the cardiovascular events after percutaneous transluminal coronary intervention (PCI) and the influence of fluvastatin on inflammation factors and prognosis of PCI patients.Methods One hundred and eighty-seven patients whose coronary stenosis ≥ 70% diagnosed through coronarography and underwent PCI from Jun.2005 to Feb.2008 were recruited in the current study.These patients were divided into two groups,the control group (n =91) was treated regularly and the treat group (n =96) was treated with additionally fluvastatin(40 mg/d).Fasting venous blood was obtained before and after medicine treatment,12,24 hours and two weeks after PCI.IL-18,IL-6 and TNF-α were measured through ELISA.Results Before medicine treatment,there were no difference of IL-18 ,IL-6 and TNF-α between the two groups( P ＞ 0.05 ).After medicine treatment,IL-18,TNF-α and IL-6 decreased significantly compared to those before treatment in both groups ( P ＜ 0.05 ),and these measurements decreased more in the treatment group ( P ＜ 0.01 ).At the 12th hours after PCI,IL-18,TNF-αand IL-6 in the control group increased to (423.5 ± 298.7 ),( 316.1 ± 72.6 ) and (42.3 ± 10.1 ) ng/L,respectively,and arrived the peak at the 24th hour,which were significantly higher than those before medicine treatment( P ＜ 0.01 ).In the treatment group,these measurements at the 12th and 24th hour after PCI were slightly higher than those before medicine treatment without significant difference ( P ＞ 0.05 ).After 12 hours ofPCI,IL- 18,TNF -αand IL-6were (276.5 ± 189.4 ),( 175.3 ± 51.9) and ( 10.1 ± 8.1 ) ng/L,which were significantly lower than those in the control group(P ＜ 0.01 ).Two weeks after PCI,IL-18,TNF-α and IL-6 in the treatment group were (137.0 ±34.2),(35.1 ± 21.6) and ( 8.7 ± 3.2 ) ng/L,which were significantly lower than before medicine treatment ( P ＜0.01 ).Conclusions PCI may aggravate the inflammation response of coronary artery.Statins may alleviate the inflammation response.IL-18,TNF-α and IL-6 are sensitive indices of early inflammation response after PCI,their changes might have prediction value for adverse cardiovascular events.Therefore these indices might be used as a target in the statins treatment in the primary prevention,as well as the evaluation of the effectiveness of PCI,statins and joint PCI and statins.
