Comparative study on the diagnostic effect of combined detection of plasma cleavage protein 9 and multi ligand proteoglycan 2 precursor methylation and four serum tumor markers for colorectal cancer / 中国综合临床

Objective:To compare the difference between the combined diagnostic effect of plasma Septin9(SEPT9) and polyligand Syndecan-2(SDC2) methylation with four serum tumor markers in the diagnosis of colorectal cancer.Methods:In this study, 128 patients who were treated in the affiliated Hospital of Xuzhou Medical University from March to December in 2019 were selected for a case-control study.All the subjects were examined by gastroenteroscopy.According to the pathological results, they were divided into three groups: colorectal cancer group( n=74) and colorectal adenoma group( n=7). The patients with no abnormal or inflammatory polyps or proliferative polyps examined by gastroenteroscopy were taken as the control group( n=47). The methylation levels of SEPT9 gene and SDC2 gene were detected by Roche Lightcycler 480 II real-time fluorescence quantitative polymerase chain reaction, and the concentrations of alpha-fetoprotein, carcinoembryonic antigen, carbohydrate antigen 125 and carbohydrate antigen 199 were detected by Roche Cobas 8000 electrochemiluminescence instrument.Chi-square test was used to compare the positive rate of each marker in the three groups.Medcalc was used to draw the receiver operating characteristic curve (ROC) curve of the subjects′ working characteristic curve, and the value of each index in the diagnosis of colorectal cancer was analyzed. Results:The positive rates of SEPT9 gene and SDC2 gene methylation were 81.1%(60/74) and 67.6%(50/74) respectively in colorectal cancer group, and increased to 85.1%(63/74) after combined detection.The positive detection rates of alpha-fetoprotein, carcinoembryonic antigen, carbohydrate antigen 125 and carbohydrate antigen 199 in colorectal cancer group were 1.4%(1/74), 33.8%(25/74), 6.8%(5/74) and 13.5%(10/74), respectively.When the four tumor markers were detected together, the positive detection rates were only increased to 43.2%(32/74), except for AFP and carbohydrate antigen 125(χ 2=3.847, 2.430, all P>0.05). The differences were statistically significant (χ 2=48.230, 30.487, 43.285, 3.847, 8.788, 6.988, 8.722, all P<0.05). The area under the curve (AUC) of SEPT9 methylation, SDC2 methylation, alpha fetoprotein, carcinoembryonic antigen, carbohydrate antigen 125 and carbohydrate antigen 199 were 0.854 (0.781, 0.910), 0.795 (0.715, 0.861), 0.575 (0.485, 0.662), 0.685 (0.597, 0.764), 0.603 (0.513, 0.689) and 0.631 (0.541, 0.715), respectively.The AUC of combined detection of two DNA methylation markers was better than that of alpha fetoprotein, carcinoembryonic antigen, carbohydrate antigen 125 and carbohydrate antigen 199, and the differences were statistically significant (alpha fetoprotein: Z=4.990, P<0.001; carcinoembryonic antigen: Z=3.743, P<0.001; carbohydrate antigen 125: Z=4.951, P<0.001; carbohydrate antigen 199: Z=3.983, P<0.001). The combined detection of two kinds of gene methylation was better than the combined detection of four kinds of serum markers in the diagnosis of colorectal cancer, and the difference was statistically significant ( Z=3.334, P<0.001). Conclusion:The combined detection of SEPT9 gene and SDC2 gene methylation in plasma is more suitable for non-invasive diagnosis of colorectal cancer than the combined detection of 4 serum tumor markers.

Analysis of risk factors for incomplete whole small intestine examination by capsule endoscopy / 中国综合临床

Objective:To explore the clinical characteristics and risk factors of incomplete endoscopy of small intestine capsule.Methods:From August 2015 to February 2019, the data of 282 patients with small intestine examination by capsule endoscopy in Affiliated Hospital of Xuzhou Medical University were analyzed retrospectively.The clinical and laboratory examination data were statistically analyzed.The risk factors of incomplete small intestine examination were analyzed by multivariate logistic regression.Results:In all 282 patients, 45 cases did not complete the examination, the incomplete rate was 16.0% (45/282). Multivariate analysis showed that male ( OR=3.261, 95% CI1.084-9.815, P=0.035), age (64.78±13.23) years ( OR=1.046, 95% CI1.007-1.086, P=0.020), intragastric time (59.78 (27.89, 108.67)) min ( OR=1.014, 95% CI1.005-1.024, P=0.004), gastrointestinal bleeding ( OR=3.017, 95% CI1.025-8.880, P=0.045), abdominal operation history ( OR=4.902, 95% CI1.553-15.470, P=0.007) were risk factors for incomplete examination.Hemoglobin (95.20±26.16) g/L( OR=0.977, 95% CI0.957-0.998, P=0.033), albumin (35.73±7.11) g/L( OR=0.871, 95% CI0.790-0.961, P=0.006) were protective factors for incomplete examination. Conclusion:Male, age, intragastric time, gastrointestinal hemorrhage and abdominal operation history were risk factors for incomplete small bowel examination with capsule endoscopy, and hemoglobin and albumin were protective factors.Before capsule endoscopy, patients should not only evaluate the intestinal stenosis, but also pay attention to the nutritional status and clinical symptoms of patients, so as to improve the completion rate of patients.

Effects and mechanism of injection of glutamate into hypothalamic paraventricular nucleus on visceral pain in chronic visceral hypersensitivity rats / 中华行为医学与脑科学杂志

Objective@#To investigate the effects of glutamate (Glu) injected into hypothalamic paraventricular nucleus (PVN) on visceral pain of chronic visceral hypersensitivity (CVH) rats and its possible mechanism.@*Methods@#Newborn SD rats were given CVH rat model by colorectal distension (CRD) on the 8th, 10th and 12th day after birth. Thirty rats with successful CVH model were randomly divided into CVH model group (CVH group), CVH + injection of saline into PVN group (NS group), CVH+ injection of Glu into PVN (3, 6, and 12 μg Glu, namely G3, G6, and G12, respectively), 6 rats in each group, and 6 SD rats with matching body mass were taken as sham operation group (Sham group). The pain behavior of the rats was evaluated by pain threshold, abdominal withdrawal reflex (AWR) score, and abdominal external oblique muscle electromyography (EMG). The expression of arginine vasopressin (AVP) and the proliferation of colon tissue were detected by immunohistochemical staining. The apoptosis of colon tissue was detected by TUNEL.@*Results@#Compared with the NS group, the pain thresholds of the G3, G6 and G12 groups increased, and the AWR scores and EMG amplitudes decreased. The differences were statistically significant(Pain threshold: t=7.65, 16.31, 24.78, both P<0.05; AWR scores: t=-2.98, -4.77, -7.29, both P<0.05; EMG amplitudes: t=-3.06, -5.75, -8.92, both P<0.05). Compared with the Sham group, the expression of AVP in PVN of the CVH group and NS group decreased ((42.63±5.20) %, (18.67±2.94) %, (17.53±2.47) %; t=6.95, t=7.56, both P<0.05). The expression of AVP was increased after different doses of Glu into PVN, and the AVP level in G12 group ((18.15±6.49)%) was higher than that of NS group, the difference was statistically significant (t=-4.21, P<0.05). Compared with the Sham group, the expression of PCNA in colonic mucosal cells of the CVH group and NS group decreased ((65.48±1.68) %, (18.39±1.67) %, (17.69±1.68) %; t=34.35, t=34.80, both P<0.05). The expression of PCNA was increased after different doses of Glu injected into PVN, and the PCNA level in G12 group ((59.91±5.63)%) was higher than that of NS group, the difference was statistically significant (t=-12.44, P<0.05). Compared with the Sham group, the expression of apoptotic cells in colonic mucosal cells of the CVH group and NS group increased ((23.38±11.40)%, (83.79±3.57)%, (80.91±2.47)%; t=-8.77, t=-8.54, both P<0.05). The expression of apoptotic cells was decreased after different doses of Glu into PVN, and the G12 group was ((18.15±6.49) %). Compared with NS group, the difference was statistically significant (t=15.65, P<0.05).@*Conclusion@#Injection of Glu into hypothalamic PVN can alleviate the visceral pain behaviors in CVH rats, and its mechanism may be related to arginine vasopressin.

Relationship between colorectal polyps and Helicobacter pylori typing and serum gastrin 17 / 中国综合临床

Objective To investigate the relationship between Helicobacter pylori infection and serum gastrin 17 levels and colorectal polyps. Methods The clinical data of 214 patients with colorectal polyps who underwent gastrointestinal endoscopy at the Affiliated Hospital of Xuzhou Medical University from June 2017 to April 2019 were collected. The specimens were divided into two groups after pathological diagnosis. The group included 126 cases with adenomatous polyps (adenomatous polyps group) and 88 cases with hyperplastic polyps( hyperplastic polyps group) . Another 89 patients without obvious abnormality were selected as the control group. Serum Hp antibody was detected by western blot,and serum gastrin 17 levels were quantitatively detected by ELISA. Hp infection rate and serum gastrin 17 levels were compared between the groups. Results The infection rate of 74. 2%( 66 ／ 89) type I HP in adenomatous polyp group was significantly higher than that of 55. 6%( 30 ／ 54) in proliferative polyp group and 48. 7%( 19 ／ 39) in control group,the difference was statistically significant( χ2＝5. 271,P＝0. 022; χ2＝7. 867,P＝0. 005). The infection rate of type I HP in proliferative polyp group was not statistically significant ( P＞0. 05) . The HP infection rate in colorectal polyp group was 66. 8%(143 ／ 214) and 67. 1%(96 ／ 143) respectively,which was significantly higher than that in control group (43. 8%(39 ／ 89) and 48. 7%(19 ／ 39),the difference was statistically significant ( χ2 ＝ 13. 87, 4. 467, all P＜0. 05 ) . The infection rate of Hp in colorectal proliferative polyp group was 61. 4%(54／88) and adenomatous polyp group was 70. 6%(89／126) higher than that in control group (43. 8%(39／89),the difference was statistically significant( χ2＝5. 46,15. 57,all P＜0. 05) . The serum gastrin 17 level in adenomatous polyp group (11. 35 ( 6. 67,20. 87) pmol／L) was significantly higher than that in proliferative polyp group (7. 88(3. 11,13. 07) pmol／L) and control group (5. 69 (2. 94,11. 37) pmol／L), the difference was statistically significant ( Z＝4. 91, all P＜0. 05) . The serum gastrin 17 level in adenomatous polyps group with type I Hp infection (14. 35 (8. 12,23. 68) pmol／L) was significantly higher than that of Hp-negative patients ( 8. 42 ( 2. 42, 20. 84) pmol／L), and the difference was statistically significant (Z＝2. 87,P＜0. 05). Conclusion HP infection is closely related to colorectal polyps,especially adenomatous polyps. The increased level of serum gastrin 17 is a risk factor for colorectal adenomatous polyps. Type I HP infection can increase the level of serum gastrin 17,and it is more closely related to adenomatous polyps.

Effects and mechanism of injection of glutamate into hypothalamic paraventricular nucleus on viscer-al pain in chronic visceral hypersensitivity rats / 中华行为医学与脑科学杂志

Objective To investigate the effects of glutamate (Glu) injected into hypothalamic pa-raventricular nucleus (PVN) on visceral pain of chronic visceral hypersensitivity (CVH) rats and its possi-ble mechanism. Methods Newborn SD rats were given CVH rat model by colorectal distension (CRD) on the 8th,10th and 12th day after birth. Thirty rats with successful CVH model were randomly divided into CVH model group (CVH group),CVH + injection of saline into PVN group (NS group),CVH+ injection of Glu into PVN (3,6,and 12 μg Glu,namely G3,G6,and G12,respectively),6 rats in each group,and 6 SD rats with matching body mass were taken as sham operation group (Sham group). The pain behavior of the rats was evaluated by pain threshold,abdominal withdrawal reflex (AWR) score,and abdominal external ob-lique muscle electromyography (EMG). The expression of arginine vasopressin (AVP) and the proliferation of colon tissue were detected by immunohistochemical staining. The apoptosis of colon tissue was detected by TUNEL. Results Compared with the NS group, the pain thresholds of the G3, G6 and G12 groups in-creased,and the AWR scores and EMG amplitudes decreased. The differences were statistically significant (Pain threshold:t=7. 65,16. 31,24. 78,both P<0. 05;AWR scores:t=-2. 98,-4. 77,-7. 29,both P<0. 05;EMG amplitudes:t=-3. 06,-5. 75,-8. 92,both P<0. 05). Compared with the Sham group,the expression of AVP in PVN of the CVH group and NS group decreased ((42. 63±5. 20) %,(18. 67±2. 94) %,(17. 53± 2. 47) %; t=6. 95,t=7. 56,both P<0. 05). The expression of AVP was increased after different doses of Glu into PVN,and the AVP level in G12 group ((18. 15±6. 49)%) was higher than that of NS group,the difference was statistically significant (t=-4. 21,P<0. 05). Compared with the Sham group,the expression of PCNA in colonic mucosal cells of the CVH group and NS group decreased ((65. 48±1. 68) %,(18. 39± 1. 67) %,(17. 69±1. 68) %;t=34. 35,t=34. 80,both P<0. 05). The expression of PCNA was increased after different doses of Glu injected into PVN,and the PCNA level in G12 group ((59. 91±5. 63)%) was higher than that of NS group,the difference was statistically significant (t=-12. 44,P<0. 05). Compared with the Sham group,the expression of apoptotic cells in colonic mucosal cells of the CVH group and NS group increased ((23. 38±11. 40)%,(83. 79± 3. 57)%,(80. 91± 2. 47)%;t=-8. 77,t=-8. 54,both P<0. 05). The expression of apoptotic cells was decreased after different doses of Glu into PVN,and the G12 group was ((18. 15±6. 49) %). Compared with NS group,the difference was statistically significant ( t=15. 65,P<0. 05). Conclusion Injection of Glu into hypothalamic PVN can alleviate the visceral pain be-haviors in CVH rats,and its mechanism may be related to arginine vasopressin.

Analysis of serum gastric function and Helicobacter pylori infection in patients with gastric hyperplastic polyps and gastric fundic gland polyps / 中国综合临床

Objective To analyze the serum gastric function and Helicobacter pylori ( HP ) infection in patients with gastric hyperplastic polyps and gastric fundic gland polyps.Methods From December 2017 to December 2018, 135 patients with gastric polyps and pathologically confirmed gastric hyperplastic polyps and gastric fundic gland polyps were enrolled in the hospital of Xuzhou Medical University.Among them, 68 patients with hyperplastic polyps, 67 cases of the gastric fundic gland polyps.Serum Hp antibodies ( UreA, UreB, VacA, CagA antibodies ) were qualitatively detected by immunoblotting.Eighty patients with chronic superficial gastritis were selected as the control group.Three groups of serum pepsinogen?I ( PG?I),pepsinogen?Ⅱ( PG?Ⅱ),gastrin were detected by enzyme?linked immunosorbent assay (ELISA).Gastrin?17( G?17) and calculate PGⅠ and PGⅡ ratio( PGR).Results The levels of serum PGⅡ(13.13(8.15,20.30) μg ／L) and G17 (8.44(3.72,27.17) pmol／L) in the gastric hyperplastic polyp group were higher than those in the control group (9.16(5.56,15.14) μg／L and 1.83(0.87,5.95) pmol／L) ( P＜0.05),and the PGR level was lower than the control group ( P＜0.05);serum PGI ( 120.12 ( 86.72,174.70) μg／L), PGII ( 11.92 ( 7.27,22.26) μg／L),G17 ( 5.68 ( 1.79, 14.65) pmol／L) in the gastric fundic gland polyp group was higher than the control group (( 101.32 (79.17,131.33) μg ／L,9.16 ( 5.56,15.14) μg ／L,1.83 ( 0.87,5.95) pmol／L) ( P 均＜0.05)) ( P＜0.05); serum G17 (8.44(3.72,27.17) pmol／L) level in gastric hyperplastic polyp group was higher than gastric fundus polyp group (5.68(1.79,14.65) pmol／L) ( P＜0.05); Hp infection rate in gastric hyperplastic polyp group61.76%(42／68)was higher than that in the gastric fundic gland polyp group40.30%(27／67) (P＜0.05),and type I Hp was the main one (P＜0.05).The serum PGⅡ and G17 levels in the gastric hyperplastic polyp group were higher than those of Hp negative ( all P＜0.05).There were no significant differences in serum PGI, PGⅡ, G17, and PGR levels between the HP?positive and negative?positive patients in the gastric fundus polyp group.The serum PGI and PGR levels in the hypertrophic polyp group were higher than those in the HPⅡ type ( all P＜0.05).There was no significant difference in the levels of serum PGⅠ,PGⅡ,G17,and PGR between the gastric fundic gland polyps group and the type Ⅱ.Conclusion Serum PG and G17 levels in patients with gastric hypertrophic polyps and gastric fundic gland polyps are higher than those in patients with chronic superficial gastritis.Patients with gastric hyperplastic polyps have higher HP infection rate and abnormal gastric function than gastric fundic gland polyps.

Effects of NANOG/deleted in breast cancer 1 pathway on biological behavior of gastric cancer cells / 中华消化杂志

Objective To investigate the effects of NANOG/deleted in breast cancer 1 (DBC1)pathway on biological behavior of gastric cancer cells.Methods From May 2014 to May 2015,25 patients who underwent gastric cancer resection were selected.The expression of NANOG and DBC1 was detected by real time reverse transcription polymerase chain reaction (RT-PCR) and Western blotting in N-tera,SGC-7901,HGC-27,MKN-45,MGC803,NCI-N87,BGC823 cell lines,normal gastric epithelial cell line GES-1 and gastric cancer tissues.The proliferation,apoptosis and colony formation ability of MKN-45 cells in short hairpin (sh)NANOG-1,shNANOG-2,sh-control and shDBC1 groups were determined by MTT assay,flow cytometry and colony forming assay.The effects on the expression of the two genes in MKN-45 cells were verified by polymerase chain reaction (PCR) in shNANOG,sh-control,shDBC1 and shDBC1+NANOG groups and the effects of down regulation of DBC1 on cell biological behavior were further investigated.The differences in gene expression profile after interference which were screened by gene chips and bioinformatics were analyzed.The mechanism of NANOG regulating DBC1 was explored by Dual-luciferase assay.T test was used for two groups comparison while one-way analysis of variance was for multiple groups.Results NANOG and NANOG mRNA were highly expressed in N-tera cells,which were 1.02±0.08 and 0.95 ±0.03,respectively,and the expressions in SGC-7901,HGC-27,MKN-45 and NCI-N87 cell lines were 0.67±0.03 and 0.64±0.04,0.58±0.02 and 0.28±0.02,0.83±0.03 and 1.04 ± 0.05,and 0.61 ± 0.02 and 0.64 ± 0.08,respectively;no expression was detected in normal gastric epithelial cell line GES-1,and the expressions in MKN-45 cells were the highest in gastric cancer cells (F=21.51 and 85.53,both P＜0.01).The expression of DBC1 in HGC-27,MGC803,NCIN87,SGC-7901,BGC823 and MKN-45 cells were 0.37±0.02,0.33±0.02,0.42±0.01,0.58±0.04,0.33±0.05,and 0.87±0.02,respectively;while there was no expression of NANOG,NANOG mRNA and DBC1 in GES-1 cells.The expression of NANOG mRNA and DBC1 was detected in gastric cancer tissues of 24.0％ (6/25) patients.Compared with that of the sh control group,the apoptosis rates of MKN-45 cells in the shNANOG-1,shNANOG-2 groups were increased ((2.24±0.17)％ vs (6.03±0.24) ％ and (6.95 ± 0.38) ％),and the difference was statistically significant (F =81.18,P ＜ 0.01).Compared with that of the sh-eontrol group,the colony forming abilities of MKN-45 cells in the shNANOG-1 and shNANOG-2 groups were significantly decreased (172.03±6.35 vs 74.32±5.32 and 53.08±3.82),and the difference was statistically significant(F=171.61,P＜0.01).The results of PCR showed that compared with that of sh-eontrol group,the expression levels of NANOG mRNA and DBC1 mRNA in shNANOG group were lower (1.04±0.05 vs 0.54±0.03,1.08±0.08 vs 0.42±0.03),the level of DBC1 mRNA in shDBC1 group was lower (1.08±0.08 vs 0.50±0.04),and the differences were statistically significant (t=9.15,7.37 and 6.06,all P＜0.01).The expression level of NANOG mRNA in shDBC1 + NANOG group was higher (1.04 ± 0.05 vs 3.01 ± 0.08),while the expression level of DBC1 mRNA was lower (1.08 ± 0.08 vs 0.71 ± 0.06),and the difference was statistically significant (t=-20.22 and 3.74,both P＜0.05).The expression level of DBC1 mRNA in shDBC1±NANOG group was higher than that in shDBC1 group (0.71±0.06 vs 0.50±0.04),and the difference was statistically significant (t=4.00,P＜0.05).Bioinformatic analysis showed that DBC1 gene promoter region had the potential NANOG protein binding sites.Dual-luciferase assay indicated NANOG played the role in transcription activation in DBC1 promoter regions.Conclusion NANOG and DBC1 are highly expressed in various gastric cancer cell lines.NANOG may affect the proliferation,apoptosis and colony formation of MKN-45 cells by regulating the expression of DBC1.NANOG/DBC1 pathway may be a promising new target of gastric cancer treatment.

Effect and Mechanism of Glutamic Acid Injection Into Cerebellar Fastigial Nucleus on Chronic Visceral Hypersensitivity in Rats / 胃肠病学

Background:Cerebellar fastigial nucleus (FN)is involved in regulation of visceral activities such as cardiovascular, ingestion,respiratory,and acute gastric mucosal injury,yet it is unclear whether it participates in the regulation of visceral hypersensitivity and what is the possible mechanism. Aims:To investigate the effect and possible mechanism of glutamic acid (Glu ) injection into cerebellar FN on chronic visceral hypersensitivity in rats. Methods: Chronic visceral hypersensitivity rat model was established by neonatal colorectal distension (CRD). After 8 weeks,the rats were divided into CRD group,solvent group (0. 2 μL 0. 9% NaCl solution injection into cerebellar FN),high-,medium-,low-dose Glu groups (12,6,3 μg Glu injection into cerebellar FN,respectively),3-MPA +Glu group (12 μg Glu injection after glutamate decarboxylase inhibitor 3-MPA injection into cerebellar FN),Bic + Glu group (12 μg Glu injection into cerebellar FN after GABAAreceptor blocker Bic injection into lateral hypothalamic area). Pain threshold,abdominal withdrawal reflex (AWR)score and abdominal external oblique muscle electromyography (EMG)were used to detect visceral sensitivity,and malondialdehyde (MDA)content and superoxide dismutase (SOD)activity were measured. Results:Chronic visceral hypersensitivity rat model was successfully established. Compared with CRD group,pain threshold was significantly increased (P＜0. 05),AWR score,EMG amplitude,MDA content were significantly decreased (P＜0. 05 ),and SOD activity was significantly increased in a dose-dependent manner in Glu group (P ＜0. 05 ). Compared with 12 μg Glu group,pain threshold was significantly decreased (P＜0. 05),AWR score,EMG amplitude, MDA content were significantly increased (P ＜0. 05),and SOD activity was significantly decreased in 3-MPA +Glu group,Bic+Glu group (P＜0. 05). Conclusions:Glu injection into cerebellar FN can significantly reduce the visceral sensitivity in rats. The mechanism may be that Glu in cerebellar FN produces GABA via glutamate decarboxylase,and then binding GABAAreceptor in lateral hypothalamic area,resulting in increased intestinal mucosal antioxidant capacity, thereby reducing visceral hypersensitivity.

Meta Analysis of Efficacy of Kangfuxin Liquid in the Treatment of Chronic Atrophic Gastritis / 医学研究杂志

Objective To evaluate the clinical effectiveness treatment of chronic gastritis by Kangfuxin liquid.Methods Computer -based online was used to retrieve Cochrane library,PubMed,CNKI,Wanfang data,VIP database(since build library retrieval time),to find the Kangfuxin liquid and add and subtract randomized controlled trials for the treatment of CAG Meta analysis was performed to evaluate the data by using RevMan5.3 software.Results Six articles were included in the study,a total of 742 patients.Meta analysis results showed that the total effective rate of Kangfuxin liquid in the treatment of chronic atrophic gastritis was better than that of routine drugs (OR =6.00,95 ％ CI:3.65-9.86,P ＜ 0.05).The helicobacter pylori eradication rate of Kangfuxin liquid in the treatment of chronic atrophic gastritis was better than that of routine drugs(OR =3.71,95％ CI:1.89-7.29,P ＜ 0.05).The effect of Kangfuxin liquid together with traditional triple therapy was better than traditional triple therapy (OR =6.15,95 ％ CI:3.24-11.68,P ＜ 0.05).Conclusion The effect of Kangfuxin liquid in the treatment of chronic atrophic gastritis is more outstanding than conventional drug treatment.

Effect and mechanism of atorvastatin on cytotoxicity of human NK cells to colon cancer cells / 中国免疫学杂志

Objective:To explore the mechanism of the cytotoxicity of human NK cells induced by atorvastatin to colon cancer cell lines. Methods:After colon cancer cells (HCT-116,SW-480,Caco-2) were cultured with different concentrations of atorvastatin, CCK-8 assay was used to assess the effect of atorvastatin on growth of colon cancer cells. The amplification of human NK cells was induced by SCGM medium in vitro. Automatic biochemical analyzer was applied to test the cytotoxicity of NK cells to colon cancer cells which cultured with different concentration of atorvastatin. FCM was used to detect the expression rate of MICA/B on the cells. Results:(1) The cultivation of NK cells:The proportion of NK cells attained to 93. 1% from 4. 5% after cultured for 10 days. (2) The effects of atorvastatin on the growth of the colon cancer cells:After cultured with atorvastatin,the inhibition rate of HCT-116 cells was higher than that in control when the density of atorvastatin increased from 5 μmol/L to 40 μmol/L after 48 h and from 1. 25 μmol/L to 40 μmol/L after 96 h ( P<0. 05 ) . Correlation analysis showed that the concentration of atorvastatin and the growth inhibition rate of HCT-116 cells were positively correlated(r[48 h]=0. 13,r[96 h]=0. 22,P<0. 05). (3) The cytotoxicity of NK cells to colon cancer cells effected after atorvastatin: In different atorvastatin concentrations groups,the cytotoxicity of NK cells to three colon cancer cell lines was all higher than that in control ( P<0. 05 ) . The atorvastatin concentration was from 2. 5 μmol/L to 10 μmol/L for HCT-116 cells,from 5 μmol/L to 20μmol/L for SW-480 cells,and from 2. 5μmol/L to 20μmol/L for Caco-2 cells. Among the three cell lines, the cytotoxicity of NK cells to HCT116 was the highest in the same concentration. (4)NK cells by atorvastatin cutting statins 96 h,the concentration of 20 mmol/L and 40 mmol/L inhibition rate was higher than that of control group,more than other groups on NK cell growth without significant effect. ( 5 ) The impact of atorvastatin on MICA/B expression of colon cancer cells: After cultured with different concentrations of atorvastatin,the expression of MICA/B on colon cancer cells was higher than that in control(P<0. 05). The concentration was 2. 5μmol/L and 5μmol/L for HCT-116 cells,10μmol/L and 20μmol/L for SW-480 cells,and from 2. 5μmol/L to 40 μmol/L for Caco-2 cells. Conclusion:Atorvastatin could inhibit the growth of colon cancer cells (HCT-116,SW-480 and Caco-2) in a dose-dependent manner;and it could enhance the cytotoxicity of NK cells to colon cancer cells;it also could promote the expression of MICA/B of colon cancer cells,and improve the immunogenicity of colon cancer cells.

A Meta-analysis of Bifidobacterium viable triple capsule on Helicobacter py lori eradication during clinical therapy / 药学实践杂志

Objective To evaluate the effecacy of Bifidobacterium viable triple capsule on anti-Helicobacter pylori (Hp) treatment and its adverse reactions during eradication therapy .Methods T rials on the effect of Bifidobacterium viable triple capsule on Hp eradication were analyzed by Meta-analysis with the software Stata 12 .0 for comprehensive quantitative analysis of its clinical efficacy and adverse reactions during treatment .Results Eight randomly controlled trials (n=114 4) were includ-ed .Pooled Hp eradication rates were 85.91% and 69 .21% for patients with and without Bifidobacterium viable triple capsule respectively ,with the odds ratio (OR) being 3 .07 (95% CI=2 .25~4 .19 ,test for overall effect Z= 7 .08 , P<0 .01);the occurrences of total adverse reactions were 7 .58% and 20.87% respectively ,with the summary OR being 0 .42 (95% CI=0 .29~0 .61 ,test for overall effect Z= 4 .48 , P< 0 .01) .The difference of the two groups was statistically significant . Conclusion Current evidence shows that Bifidobacterium viable triple capsule could increase eradication rate of anti-Hp treat-ment and improve adverse reactions during therapy .

Protective Effect and its Mechanism of Galanin Receptor 2 Agonist Post-conditioning on Human Gastric Epithelial Cells Injury Induced by Hypoxia/Reoxygenation / 胃肠病学

Background:Gastric ischemia-reperfusion injury often leads to calcium overload,excessive free radical production, leukocyte infiltration and microcirculation disturbance.Post hypoxic treatment can effectively reduce the injury induced by hypoxia/reoxygenation (H/R).Galanin receptor 2 (GalR2)is distributed mainly in the digestive and nervous system, which can regulate many endocrine activity.However,the protective effect of GalR2 on human gastric epithelial cells injury induced by H/R is not clarified.Aims:To investigate the protective effect and its mechanism of GalR2 agonist post-conditioning on human gastric epithelial cells injury induced by H/R.Methods:H/R model was constructed on human gastric epithelial cells GES-1.Normal control group (N group),H/R group,M1145 (GalR2 agonist)treatment group (M group),SB203580 (p38MAPK inhibitor) +M1145 treatment group (S +Mgroup)and DMSO solvent control group (D group)were established.Survival rate of cells was measured by MTT assay.Apoptosis rate of cells was determined by flow cytometry,and cell apoptosis was examined by Hoechst staining.Level of lactate dehydrogenase (LDH)was measured by ELISA.Expressions of Bcl-2,Bax and p38MAPK were determined by real-time quantitative PCR.Results:Survival rate of cells was significantly lower in H/R group than that in N and M groups (P <0.05 ).Apoptosis rate of cells was significantly higher in H/R group than that in N,M and S +M groups (P <0.05 ),and apoptosis rate of cells was significantly lower in Mgroup than that in S +M group (P <0.05).Expression of LDH was significantly higher in H/R group than that in Mand S +Mgroups (P <0.05).Expression of Bcl-2 was significantly higher in N and M groups than that in H/R,S +Mand D groups (P <0.05);expression of Bax was significantly higher in H/R group than that in N,M and S +Mgroups (P <0.05);expression of p38MAPK was significantly lower in H/R and S +M groups than that in M group (P <0.05 ).Conclusions:GalR2 agonist M1145 plays an effective role in reducing the injury of GES-1 cells induced by H/R,the effect may be conducted through p38MAPK pathway.

Enhanced killing activity of γδT cells against SW1990 cells by dihydroartemisinin / 中华微生物学和免疫学杂志

Objective To investigate the effect of DHA on proliferation and killing activity of γδT cells against SW1990 cells in vitro.Methods γδT cells were generated in vitro by stimulating peripheral blood mononuclear cells of healthy donors in RPMI 1640 completed medium containing IPP and IL-2 for 8 d,and then co-cultured with different concentrations of DHA for 48 h.Proliferation rates of γδT cells for each group were detected by MTT method.The perforin,granzyme B and CD107a expression in γδT cells were verified by flow cytometer.The cytotoxic activity of γδT cells against SW1990 cells were analyzed by CCK-8 kit.Results The purity of γδT cells in each group reached 75.46％ ±5.32％ after 8 d of culture.Compared with the control group,the proliferative capability of γδT cells were enhanced significantly after treated with 50-100 μmol/ml DHA for 48 h,moreover,cytotoxicity against SW1990 cells and perforin,granzyme B and CD107a expression of the γδT cells treated with DHA were higher than the control group.Conclusion DHA could enhance the antitumor activity of γδT cells,which may be associated with the upregulation of perforin and granzyme B expression in γδT cells.

Effect of hydrocortisone on proliferation and killing activity of NK cells against SW1990 cells / 中华胰腺病杂志

Objective To investigate the effects of hydrocortisone (HC) on proliferation and killing activity of NK cells against pancreatic cancer SW1990 cells in vitro.Methods Peripheral blood mononuclear cells of healthy people were isolated and cultured with NK cells medium containing IL-1S.When the purity of NK cells reached above 70％,different concentrations of HC (10-6,10-5,10-4,10-3 μmol/L) were added and co-cultured with NK cells for 7 days.And NK cells without HC were used as control.CD3-CD56 + NK cell numbers of each group were countered by trypan blue staining.Perforin,granzyme B and IFN-γ expression of CD3-CD56+ + NK cells were verified by flow cytometry.NK cells and SW1990 cells were co-cultured with a 20∶1effector to target ratio,then the cytotoxic activity of NK cells against SW1990 cells were analyzed by CCK-8 kit.Results After treatment with different concentration of HC for 7 days,NK cells purity of each group reached 70.72％ ～ 76.39％,and it was not significantly different with that in control group [(72.61 ± 3.76) ％].The proliferation folds of NK cells treated with 10-6,10-5,10-4,10-3 μmol/L HC were (9.13 ± 0.94),(9.67 ±1.51),(10.33±1.07),(8.40±1.47) times,respectively,while it was (4.23 ±0.82) times in control group (all P ＜0.01).The killing effects of NK cells on SW1990 cells were (58.58 ± 4.89) ％,(62.27 ± 5.63) ％,(64.02 ± 5.79) ％,(63.88 ± 3.61) ％,which were higher than that in control group [(57.46 ± 5.11) ％],moreover,the difference between NK cells of 10-4 μmol/L HC treatment group and control group was statistically significant(P ＜ 0.05).The expressions of perforins of 10-4,10-3 μmol/L HC treatment group were (96.71 ± 3.04) ％,(97.56 ± 2.18) ％,which were significantly higher than that in control group [(92.40 ±3.53)％,P ＜0.05 or 0.01].The expression of granzyme B in 10-5 μmol/L HC treatment group was (78.23 ±2.94)％,which were significantly higher than that in control group [(73.68 ±3.52) ％,P ＜0.05].The expressions of IFN-γ in 10-5,10-4,10-3 μmol/L HC treatment group were (96.61 ±2.04)％,(97.58 ± 2.17)％,(98.00 ± 1.77)％,which were significantly higher than that in control group [(92.44 ± 2.74)％,P＜0.01].Conclusions HC can promote IL-15 activated NK cells proliferation and enhance NK cells mediated killing activity against SW1990 cells with proper concentration,and up-regulation of perforin,granzyme B and IFN-γ expression may be the main mechanisms.

Expression of interleukin-22 and relative CD4+ T cell subsets in ulcerative colitis / 中华微生物学和免疫学杂志

Objective To detect the expression of interlenkin-22 (IL-22) and relative CD4+ T cell subsets in patients with ulcerative colitis (UC),and to explore their roles in the pathogenesis of UC.Methods Thirty-five adult UC patients were enrolled in this study and 35 healthy subjects were taken as control.Plasma IL-22 level was quantified by ELISA.The percentages of Th1,Th17 and Th22 cells in peripheral blood were determined by flow cytometry.The relationships of these results and disease activity were analyzed.Results Plasma IL-22 levels in UC patients [ (354.12±104.22 ) pg/ml ]were significantly higher than that of healthy controls ( P＜0.05 ),and the levels increased significantly in severely active patients.The percentages of Th17 cells in UC patients [ (2.36±0.94) ％ ]were elevated compared to healthy controls ( P＜0.05 ),and the percentages increased significantly in moderately active and severely active patients.The percentages of Th22 cells in UC patients [ (2.27±0.87 ) ％ ]were elevated compared to healthy controls (P±0.05),and the percentages increased significantly in severely active patients.The percentage of Th1 cells was not significantly different between UC patients and normal controls.ConclusionOur resuits demonstrate elevated IL-22 correlated to Th17 and Th22 cells may play an important role in the immunopathogenesis of UC.

Research of mechanism about enhancing the activity of γδδT cells treated by resveratrol on colonic cancer cell lines SW-1116 / 中华微生物学和免疫学杂志

Objective To explore the effect of γδT cells on colonic cancer cell lines SW-1116 treated by resveratrol. MethodsAmplification γδT cells of human peripheral blood in vitro by using isopentenylpyrophosphate. Different density resveratrol induced γδT cells and colonic cancer cell SW-1 116, methyl thiazolyl tetrazolium(MTT) detectde the effect of growth and proliferation when expression veratrol action to γδT cells and colonic cancer cell lines SW-1116. Flow cytometer( FCM )detectde the expression of porforin, granzymeB and CD107a on γδT cells before it treated by resveratrol and after that. γδT cells against colonic cancer cell lines SW-1116 were detectde by lactate dehydrogenase(LDH) releasing assay before and after treated by resveratrol.Western blot analyzed the liveness of extracellular signal-regulated kinase1/2 of γδT cells before it treated by resveratrol and after that. ResultsγδTcells would be proliferation when the density of resveratrol in 0.39-3.125 μmol/L, while the effect on colonic cancer cell lines SW-1116 was not significance. There was significant difference of the expression of porforin, ranzymeB and CD107a on γδT cells before it treated by resveratrol and after that ( P＜0.05 ). γδT cells against colonic cancer cell lines SW-1116 treated by resveratrol was enhanced compared with control group( P＜0.05 ) . The p-ERK 1/2expression of γδT cells enhanced when the density of resveratrol treated to γδT cells in 0.1-10 μmol/L( P＜0.05 ). Conclusion Resveratrol could promote γδT cells, proliferation and strengthen the cytotoxicity of γδT cells against colonic cancer cell SW-1116, the mechanism might concerned with activating p-ERK1/2 and enhancing the expression of porforin, granzymeB and CD107a on γδT cells.

Effects of GABA on proliferation and metastasis of pancreatic cancer cell / 中华胰腺病杂志

Objective To observe the effects of GABA on proliferation, cell cycle and expression of MMP-2, MMP-9 of pancreatic cancer cell line SW1990. Methods The effects of different concentration of GABA (0 ～ 320 μmol/L) on proliferation and cell cycle of pancreatic cancer cell line SW1990 was investigated by MTT assay and flow cytometry analysis, respectively. Expressions of MMP-2 and MMP-9 proteins were evaluated by Western blot analysis. Results GABA could promote the proliferation of SW1990 cells and influence the distribution of cell cycle, which made less cells of G0/G1 phase and more cells of S and G2/M phase. The value of A570 after GABA pretreatment at a dose of 320 μmol/L was 1. 11 ± 0.03, which was significantly higher than that in the control group (0. 56 ± 0.01, P < 0. 01 ), the cells of G0/G1 phase was (46.18 ± 1.12 )% ,which was significantly lower than (87.29 ± 1.34)% in the control group (P < 0. 01 ) ;the expressions of MMP-2 mRNA, MMP-9 mRNA and their proteins were 8.6, 6.8, 10.5, 8.4, respectively, which were significantly higher than those in the groups of the doses of 0 ～ 40 μmol/L ( P < 0. 05 ). Conclusions GABA could influence the proliferation and expression of MMP of SW1990 cells.

Expression of COX-2,p53 and PCNA in esophageal carcinoma and its significance / 中国癌症杂志

Purpose:To study the expression of COX 2,P53 and PCNA in esophageal carcinomas and its significance. Methods:Immunohistochemical method was used to examine the sections from 82 esophageal squamous cell carcinomas, 20 esophagitis and 16 normal esophageal mucosa tissues. Results:The positive ratios of COX 2,p53 and PCNA were 87.8%(72/82),82.9%(68/82)and 95.1%(78/82) in 82 esophageal carcinomas, respectively. But there was no expression in adjacent noncancerous tissues and normal esophageal mucosa tissues. The positive ratio of COX 2 protein was significantly higher in the well differentiated and moderately differentiated esophageal carcinomas than in the poorly differentiated esophageal carcinomas( P

Effect of ?-aminobutyric acid on proliferation of cytokine-induced killer cells / 中国免疫学杂志

Objective:To study the effect of GABA and A receptor agonist THIP on proliferation and apoptosis of cytokine-induced killer (CIK) cells.Methods:CIK cells were cultured by routine method,and then treated with different concentrations of GABA and THIP.The proliferation of CIK cells were investigated by MTT assay.The apoptosis,cell cycle and immunophenotype were investigated by flow cytometry.Results:GABA could inhibit the proliferation of CIK cells in a dose-dependent manner and affect the distribution of cell cycle of CIK cells(P