OBJECTIVE To discuss risk factors of hospital infection in patients who suffered from primary cancer of the liver in the medium and advanced stage and give the countermeasures.METHODS The liver cancer cases in medium and advanced stage in 2001-2006 were retrospectively investigated and analyzed.RESULTS The hospital infection rate was 33.92% for the liver cancer patients who were in the medium and advanced period;the more common sites of infection were lungs,abdominal cavity,intestinal tract,blood.The motality was 20.83% in the infection group and 10.16% in non-infection group and there were significant differences between two groups(P

ObjectiveTo study the application effect of Orem self-care theory in nursing of postoperative chemotherapy patients after cervical cancer surgery. Methods60 patients receiving chemotherapy after cervical cancer surgery were randomly divided into the self-care group and the control group with 30 cases in each group,the control group received routine nursing,on this basis the self-care group was given nursing intervention according to different requirement of patients by using three nursing model of Orem self-care theory-supportive education,part compensation,complete compensation system.The nursing effect was compared between two groups. ResultsCompared with the control group,the rate of gastrointestinal adverse reaction was lower,the anxiety and depression symptom alleviated,satisfaction degree of patients and their relatives with nursing improved,self-care ability of patients was enhanced in the self-care group,all had significant differences. ConclusionsApplication of self-care theory in nursing care of patients during chemotherapy after cervical cancer can greatly mobilize the enthusiasm of patients and their families and reduce the incidence of gastrointestinal side effects.Meanwhile,it can make close nurse-patient relationship,improve the satisfaction degree of patients and their families,improve self-care capacity,improve the quality of care,reduce the psychological symptoms of patients,so it has significant social and economic benefits.

Objective To establish the sulfur mustard (SM ) induced tracheal injury model in rat and to investigate its mecha-nism .Methods Male rats (SD) were anesthetized and intra-tracheally intubated .The SM group was intra-tracheally injected by 2 mg/kg of diluted SM ,while the propylene glycol control group only by 0 .1mL of propylene glycol and the normal control group had no any treatment .The tissue and blood samples were taken for conducting the HE and immunohistochemical staining and measuring serum enzymes and andinflammatory factors .Results In the SM group ,a large number of lymphocytes infiltration in submucosa were observed;the positive expression of caspase-3 and caspase-9 were observed in epithelium and submucosa ;serum levels of TNF-α,IL-1β,IL-6 reached the peak in 24 h;serum levels of LDH ,GP ,BARS reached the peak in 6h ,so did GGT in 24 h .In the propyl-ene glycol control group and the normal control group ,lymphocytes ,macrophages and neutrophils were rare in submucosa .Conclu-sion The mechanism of SM (2 mg/kg) induced acute tracheal injury involves the inflammatory reaction ,apoptosis and oxidative stress ,moreover the lesion degree has the correlation with time .

Objective To prepare the human papillomavirus (HPV) 16 peptide vaccine and explore the effect in vitro and in vivo. Methods (1) Prediction of the major histocompatibility complex (MHC) class I restricted T cell epitopes by bioinformatics target at transporter associated with antigen processing (TAP) and named by E7Pa, E7Pb, E7Pc separately. (2)In vivo, the C57BL/6 mice were divided into five groups with same amounts randomly after loading with TC-1 cells (HPV 16 positive tumor cells from C57BL/6 mouse), named as E7Pa + CpG,E7Pb + CpG,E7Pc + CpG (as experiment groups, and added 50 μg/ml E7Pa, E7Pb, E7Pc, respectively), CpG(as positive control group and added Con A with 12 mg/L final concentration) and blank control group (without any treatment). The T cell proliferation was detected by methyl thiazolyl tetrazolium (MTT) assay at different time points;the lactate dehydrogenase (LDH) delivery method was used to test the cytolytie T lymphocyte (CTL) activity of mouse splenic lymphocyte in different ratio of effector cells and target cells (E:T);the related cytokines in tumor tissue and mouse peripheral blood were evaluated by real-time PCR and enzyme-linked immunosorbent assay (ELISA), respectively. The tumor volumes were measured to contrast the therapeutic effect in different groups. Results (1) Three peptide named E7Pa, E7Pb, E7Pc were successfully preparated which had high affinity and specificity. (2) After vaccination of 24, 48, 72,96 hours, MTT results shown that the proliferation rate in E7Pa + CpG group were(131±32)%, (302±15)%, (552±28)%, (731±24)% individually, which were much higher than those in blank control [(72± 15) %, (120 ± 57) %, (176 ±41)%, (288±29)% ;P<0.01], and the other groups i. e. E7Pb + CpG,E7Pc +CpG and CpG groups all proliferated much higher than those in blank control group with statistic signification (P<0. 05), but there was no significant difference between groups(P>0.05);the LDH delivery assay showed that when the ratio of E:T was 100:1, the activity of CTL in the E7Pa + CpG group was most powerful than the other groups with statistic signification (P<0. 01). Meanwhile, the ratio of E:T was concentration-dependent. Compared E7Pb + CpG, E7Pc + CpG or CpG groups with blank control group, there were significantly difference(P<0. 05) ,while there was no significant difference between groups(P >0. 05). The mRNA levels of interferon γ (IFN-γ), interleukin-2 (IL-2) in tumor tissue and peripheral blood in E7Pa + CpG group were significantly higher than those in blank control group (P<0. 01), which was the similar results when compared E7Pb + CpG, E7Pc + CpG or CpG groups with control group (P < 0. 05), and without significant difference between groups(P > 0. 05). The tumor volumes were suppressed obviously in all the experiment groups, especially at the 60th days, the volumes in ETPa + CpG group were much smaller than that in blank control group with statistic signification (P < 0. 01),which was the similar results that E7Pb + CpG, E7Pc + CpG or CpG groups had difference than blank control group with statistic signification (P < 0. 05), and without significant difference between groups(P >0. 05). Conclusion The HPV16 E7 peptide target at TAP combination with CpG as a vaccine could treat effectively the HPV16 E7 positive tumor in experiment.

ObjectiveTo explore the correlation between the degree of liver damage and clinical manifestations in patients with pulmonary tuberculosis after chemotherapy. MethodsThis study included 3620 new smear-positive pulmonary tuberculosis patients treated with first-line anti-tuberculosis drug in the Second Central Hospital of Baoding from January 2008 to January 2014, and the follow-up study was carried out to observe medication use and side effects of anti-tuberculosis drug treatment. Comparison of categorical data was made by chisquare test. ResultsA total of 1225 patients (33.8%) exhibited clinical manifestations related to liver injury. The most common clinical manifestation was nausea and vomiting (72.9%), followed by fatigue (37.8%), rash (31.5%), abdominal distension and diarrhea (281%), fever (14.2%), anorexia (3.8%), and other manifestations (2.0%). The nausea and vomiting usually first appeared and were followed by abdominal distension and diarrhea. Of all patients, 243 cases (6.7%) suffered from liver damage and 109 cases (3.0%) had moderate to severe liver damage. Of the patients with clinical manifestations, 171 cases (14.0%) had liver damage and 74 cases(60%) suffered from moderate to severe liver damage. Compared with the patients without clinical manifestations, the relative risks of liver damage and moderate to severe liver damage were 4.643 ［95% confidence interval (CI)=3.035-4.856］ and 4.134 (95% CI=2.817-4.351), respectively, in the patients with clinical manifestations. The patients with fatigue, nausea and vomiting, rash, abdominal distension and diarrhea, anorexia, and other manifestations had higher risk of liver damage and moderate to severe liver damage than those without clinical manifestations (P＜0.05) and the patients with anorexia showed the highest risk. ConclusionOne third of patients with pulmonary tuberculosis have liver injury-related clinical manifestations after chemotherapy. Patients with fatigue, nausea and vomiting, rash, abdominal distension and diarrhea, anorexia, and other manifestations are more susceptible to liver damage and moderate to severe liver damage.

Objective To explore the effect and mechanism of adenosine A2A receptor(A2AR)on lipopolysac-charide(LPS)-induced inflammatory injury of Caco-2 intestinal epithelial cells.Methods Caco-2 cells were di-vided into control group,LPS group(treated with 10 μg/ml LPS for 12 h),A2AR agonist(CGS21680)group(pretreated with 50 nmol/L CGS21680 for 10 min),CGS21680+LPS group(pretreated with 50 nmol/L CGS21680 for 10 min,treated with 10 μg/ml LPS for 12 h),cell viability was determined using CCK-8 assay,the secretion levels of tumor necrosis factor-α(TNF-α),interleukin-1 β(IL-1 β)and interleukin-6(IL-6)in cell su-pernatant of each group were determined using ELISA.mRNA expression levels of TNF-α,IL-1 β and IL-6 in cells of each group were detected by real-time fluorescence quantitative PCR,the protein expression levels of microtubule associated light chain protein 3(LC3)-Ⅱ/LC3-Ⅰ and autophagy associated protein(Beclin1)in cells of each group were analyzed using Western blot analysis.Caco-2 cells were then divided into control group,LPS group(pretreated with 50 nmol/L CGS21680 for 10 min),CGS21680+LPS group(pretreated with 50 nmol/L CGS21680 for 10 min,treated with 10 μg/ml LPS for 12 h),CGS21680+LPS+Rapa group(pretreated with 50 nmol/L CGS21680 for 10 min,treated with 10 μg/ml LPS and 5 μmol/L Rapa for 12 h),cell viability was deter-mined using CCK-8 assay,the secretion levels of TNF-α,IL-1 β and IL-6 in cell supernatant of each group were determined using ELISA.Results Compared with the control group,the viability of Caco-2 cells in LPS group sig-nificantly decreased(P＜0.05),the levels of TNF-α,IL-1 β and IL-6 in supernatant significantly increased(P＜0.05),the mRNA relative expressions of TNF-α,IL-1β,IL-6 in cells significantly increased(P＜0.05),the LC3-Ⅱ/LC3-Ⅰ ratio and the relative expression of Beclin1 protein were significantly up-regulated(P＜0.05).Compared with LPS group,the viability of Caco-2 cells in CGS21680+LPS group significantly increased(P＜0.05),the levels of TNF-α,IL-1 β and IL-6 in supernatant significantly decreased(P＜0.05),the mRNA rela-tive expression levels of TNF-α,IL-1β,IL-6 in cells were significantly down-regulated(P＜0.05),and the ratio of LC3-Ⅱ/LC3-Ⅰ and the relative expression of Beclin1 protein were significantly down-regulated(P＜0.05).In addition,compared with CGS21680+LPS group,the viability of Caco-2 cells in CGS21680+LPS+Rapa group significantly decreased(P＜0.05),and the levels of TNF-α,IL-1 β and IL-6 in the supernatant also significantly increased(P＜0.05).Conclusion A2 AR agonist can reduce the inflammatory injury of Caco-2 intestinal epithe-lial cells induced by LPS and improve cell viability,which may be related to its inhibition of autophagy.

OBJECTIVETo establish an animal model of sulfur mustard (SM)-induced acute lung injury in rats through different routes and compare the morphological changes in lung tissue and cells.

METHODSOne hundred and thirty-six male rats were selected and randomly divided into 5 groups, namely peritoneal cavity SM group (n=32), trachea SM group (n=32), peritoneal cavity propylene glycol group (n=32), trachea propylene glycol group (n=32), and normal control group (n=8). The rats in peritoneal cavity SM group were injected intraperitoneally with diluted SM (0.1 ml, 8 mg/kg), and the rats in trachea SM group were injected intratracheally with diluted SM (0.1 ml, 2 mg/kg). Once the rats were sacrificed at 6, 24, 48, and 72 h after SM treatment, morphological changes in lung tissue and cells were observed by light and electron microscopy.

RESULTSIn the peritoneal cavity SM group, the epithelial cells of bronchioles maintained intact with increased exudate and bleeding in alveolar cavity and large areas of pulmonary consolidation under the light microscope. In the tracheal SM group, focal ulcer formed in the epithelial cells of bronchioles with increased exudate and bleeding in alveolar cavity, partial pulmonary consolidation, and compensatory emphysema in peripheral alveolar space under the light microscope. The alveolar interval areas were widened obviously in both groups in a time-dependent manner. Under the electron microscope, we observed local loss of cellular membrane in type I alveolar epithelium, broken or lost microvilli in cells of typeⅡalveolar epithelium and fuzzy mitochondrial crista as well as the appearance of ribosome detached from rough endoplasmic reticulum in both two groups. Compared with those in the trachea SM group and the control group, the ratio of the alveolar septum average area to the visual field area in the peritoneal cavity SM group at 6, 24, 48, and 72 h was significantly higher (P<0.05).

CONCLUSIONThe lung tissue injury through the intraperitoneal route is more severe than that through the tracheal route, while focal ulceration of bronchioles epithelial cells appears in the case of tracheal route. The degree of injury increases over time in both groups, and the cellular damage is approximately the same in both groups.

Acute Lung Injury ; chemically induced ; pathology ; Animals ; Disease Models, Animal ; Lung ; pathology ; Male ; Mustard Gas ; toxicity ; Peritoneum ; Pulmonary Alveoli ; pathology ; ultrastructure ; Rats ; Trachea

Objective To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down?regulating miR?29. Methods The expression levels of HULC and miR?29 in HCC tissues and cells were detected by real?time quantitative PCR ( RT?qPCR ), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR?29 and its target gene SETDB1 were determinate by RT?qPCR. According to the bioinformatic prediction of the miR?29 binding site in the HULC sequence, the report gene plasmids were constructed.The HCC cells were co?transfected with miR?29 mimics or miR?29 inhibitor, and the HULC targeted regulation of miR?29 was verified by dual luciferase reporter assay. The effect of miR?29 on the HULC?mediated proliferation in HCC cells was detected by cell count kit 8 ( CCK?8) experiment. Expression of tumor proliferation antigen Ki?67 was detected by RT?qPCR.The Hep3B cells were inoculated in mice and miR?29 mimics and miR?29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki?67 in tumor tissues were detected by immunohistochemical staining. Results The expression of HULC was significantly up?regulated while the expression of miR?29 was significantly down?regulated in HCC tissues and cells (P＜0.01). The level of HULC was negatively correlated with miR?29 in tumor tissues (r＝－0.754, P＜0.01) and HCC cells ( r＝－0.865, P＜0.05).The in vitro experiments showed that, compared with the blank control group, the expression of miR?29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR?29 target gene SETDB1 was increased ( P＜0.01). The expression of miR?29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P＜0.01). Double luciferase reporter gene assay showed that miR?29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type ( psi?HULC?WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid ( psi?HULC?Mut). However, the miR?29 inhibitor antagonized the inhibitory effect of miR?29 mimics on luciferase activity of psi?HULC?WT (P＜0.01).Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR?29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87± 3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P＜0.05).After treatment for 48 and 72 hours, the proliferation rates of miR?29 mimics transfected Huh7 cells were ( 57.10 ± 1.94)% and ( 73.76± 3.46)%, respectively, significantly lower than (83.45±7.46)% and ( 123.34±8.67)% of control group ( P＜0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR?29 mimics and miR?29 inhibitor group were (76.45± 3.24)% and ( 89.37± 4.37)%, respectively, significant higher than (57.10%±1.94)% and ( 73.76 ± 3.46)% of the control group ( P＜0.05). After 48 h transfection, the expression of Ki?67 in Huh7 transfected with miR?29 mimics was significantly inhibited compared with the control group (P＜0.01). However, the expression of Ki?67 mRNA was increased in Huh7 cells transfected with miR?29 inhibitor (P＜0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR?29 mimics group and miR?29 mimics + miR?29 inhibitors group were ( 504.0± 19.6) mm3, (310.0±24.3) mm3 and (483.7±21.2) mm3, respectively. Injection of miR?29 mimics reduced while miR?29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P＜0.01). The immunohistochemical staining showed that the average optical density values of Ki?67 protein in tumor tissues of the control group, miR?29 mimics group and miR?29 analogue+miR?29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki?67 protein in miR?29 mimics group was significantly reduced ( P＜0.01) while increased in the miR?29 mimics+miR?29 inhibitor group ( P＜0.01). Conclusion LncRNA HULC promotes HCC growth by down?regulating miR?29.

Objective To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down?regulating miR?29. Methods The expression levels of HULC and miR?29 in HCC tissues and cells were detected by real?time quantitative PCR ( RT?qPCR ), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR?29 and its target gene SETDB1 were determinate by RT?qPCR. According to the bioinformatic prediction of the miR?29 binding site in the HULC sequence, the report gene plasmids were constructed.The HCC cells were co?transfected with miR?29 mimics or miR?29 inhibitor, and the HULC targeted regulation of miR?29 was verified by dual luciferase reporter assay. The effect of miR?29 on the HULC?mediated proliferation in HCC cells was detected by cell count kit 8 ( CCK?8) experiment. Expression of tumor proliferation antigen Ki?67 was detected by RT?qPCR.The Hep3B cells were inoculated in mice and miR?29 mimics and miR?29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki?67 in tumor tissues were detected by immunohistochemical staining. Results The expression of HULC was significantly up?regulated while the expression of miR?29 was significantly down?regulated in HCC tissues and cells (P＜0.01). The level of HULC was negatively correlated with miR?29 in tumor tissues (r＝－0.754, P＜0.01) and HCC cells ( r＝－0.865, P＜0.05).The in vitro experiments showed that, compared with the blank control group, the expression of miR?29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR?29 target gene SETDB1 was increased ( P＜0.01). The expression of miR?29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P＜0.01). Double luciferase reporter gene assay showed that miR?29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type ( psi?HULC?WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid ( psi?HULC?Mut). However, the miR?29 inhibitor antagonized the inhibitory effect of miR?29 mimics on luciferase activity of psi?HULC?WT (P＜0.01).Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR?29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87± 3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P＜0.05).After treatment for 48 and 72 hours, the proliferation rates of miR?29 mimics transfected Huh7 cells were ( 57.10 ± 1.94)% and ( 73.76± 3.46)%, respectively, significantly lower than (83.45±7.46)% and ( 123.34±8.67)% of control group ( P＜0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR?29 mimics and miR?29 inhibitor group were (76.45± 3.24)% and ( 89.37± 4.37)%, respectively, significant higher than (57.10%±1.94)% and ( 73.76 ± 3.46)% of the control group ( P＜0.05). After 48 h transfection, the expression of Ki?67 in Huh7 transfected with miR?29 mimics was significantly inhibited compared with the control group (P＜0.01). However, the expression of Ki?67 mRNA was increased in Huh7 cells transfected with miR?29 inhibitor (P＜0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR?29 mimics group and miR?29 mimics + miR?29 inhibitors group were ( 504.0± 19.6) mm3, (310.0±24.3) mm3 and (483.7±21.2) mm3, respectively. Injection of miR?29 mimics reduced while miR?29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P＜0.01). The immunohistochemical staining showed that the average optical density values of Ki?67 protein in tumor tissues of the control group, miR?29 mimics group and miR?29 analogue+miR?29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki?67 protein in miR?29 mimics group was significantly reduced ( P＜0.01) while increased in the miR?29 mimics+miR?29 inhibitor group ( P＜0.01). Conclusion LncRNA HULC promotes HCC growth by down?regulating miR?29.

Objective: To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down-regulating miR-29. Methods: The expression levels of HULC and miR-29 in HCC tissues and cells were detected by real-time quantitative PCR (RT-qPCR), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR-29 and its target gene SETDB1 were determinate by RT-qPCR. According to the bioinformatic prediction of the miR-29 binding site in the HULC sequence, the report gene plasmids were constructed. The HCC cells were co-transfected with miR-29 mimics or miR-29 inhibitor, and the HULC targeted regulation of miR-29 was verified by dual luciferase reporter assay. The effect of miR-29 on the HULC-mediated proliferation in HCC cells was detected by cell count kit 8 (CCK-8) experiment. Expression of tumor proliferation antigen Ki-67 was detected by RT-qPCR.The Hep3B cells were inoculated in mice and miR-29 mimics and miR-29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki-67 in tumor tissues were detected by immunohistochemical staining. Results: The expression of HULC was significantly up-regulated while the expression of miR-29 was significantly down-regulated in HCC tissues and cells (P<0.01). The level of HULC was negatively correlated with miR-29 in tumor tissues (r=-0.754, P<0.01) and HCC cells (r=-0.865, P<0.05). The in vitro experiments showed that, compared with the blank control group, the expression of miR-29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR-29 target gene SETDB1 was increased (P<0.01). The expression of miR-29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P<0.01). Double luciferase reporter gene assay showed that miR-29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type (psi-HULC-WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid (psi-HULC-Mut). However, the miR-29 inhibitor antagonized the inhibitory effect of miR-29 mimics on luciferase activity of psi-HULC-WT (P<0.01). Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR-29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87±3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P<0.05). After treatment for 48 and 72 hours, the proliferation rates of miR-29 mimics transfected Huh7 cells were (57.10±1.94)% and (73.76±3.46)%, respectively, significantly lower than (83.45±7.46)% and (123.34±8.67)% of control group (P<0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR-29 mimics and miR-29 inhibitor group were (76.45±3.24)% and (89.37±4.37)%, respectively, significant higher than (57.10%±1.94)% and (73.76±3.46)% of the control group (P<0.05). After 48 h transfection, the expression of Ki-67 in Huh7 transfected with miR-29 mimics was significantly inhibited compared with the control group (P<0.01). However, the expression of Ki-67 mRNA was increased in Huh7 cells transfected with miR-29 inhibitor (P<0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR-29 mimics group and miR-29 mimics + miR-29 inhibitors group were (504.0±19.6) mm³, (310.0±24.3) mm³ and (483.7±21.2) mm³, respectively. Injection of miR-29 mimics reduced while miR-29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P<0.01). The immunohistochemical staining showed that the average optical density values of Ki-67 protein in tumor tissues of the control group, miR-29 mimics group and miR-29 analogue+ miR-29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki-67 protein in miR-29 mimics group was significantly reduced (P<0.01) while increased in the miR-29 mimics+ miR-29 inhibitor group (P<0.01). Conclusion LncRNA HULC promotes HCC growth by down-regulating miR-29.