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Objective:To correlate the expression of microRNA (miRNA)-21 and miRNA-335-5p with pepsinogen and gastrin-17 in patients with gastric cancer.Methods:Sixty-one patients with gastric cancer who received treatment in Linhai Second People's Hospital between January 2019 and January 2021 were included in the patient group. An additional 60 healthy patients who concurrently received physical examination were included in the control group. Serum pepsinogen I, pepsinogen II and gastrin-17 levels were determined by latex-enhanced immunoturbidimetry. miRNA-21 and miRNA-335-5p expression were determined by quantitative reverse transcription-polymerase chain reaction. Serum pepsinogen I, pepsinogen II and gastrin-17 levels and miRNA-21 and miRNA-335-5p expression were compared between the two groups. The sensitivity and specificity of miRNA-21 and miRNA-335-5p in the diagnosis of gastric cancer were analyzed. The correlation between miRNA-21 and miRNA-335-5p expression and pepsinogen I, pepsinogen II and gastrin-17 levels was analyzed.Results:Serum pepsinogen I and gastrin-17 levels in the patient group were (54.36 ± 9.89) μg/L and (13.74 ± 1.89) pg/mL, respectively, which were significantly lower than those in the control group [(112.31 ± 23.24) μg/L, (18.75 ± 2.36) pg/mL, t = 17.89, 12.90, both P < 0.05]. Serum pepsinogen II level in the patient group was significantly higher than that in the control group [(24.35 ± 4.53) μg/L vs. (20.37 ± 3.28) μg/L, t = 5.52, P < 0.05]. The relative mRNA expression of miRNA-21 in the patient group was significantly higher than that in the control group [(3.42 ± 0.61) vs. (0.53 ± 0.12), t = 30.01, P < 0.05]. The relative mRNA expression of miRNA-335-5p in the patient group was significantly lower than that in the control group [(0.32 ± 0.17) vs. (1.65 ± 0.35), t = 26.65, P < 0.05]. The receiver operating characteristic curve analysis showed that the sensitivity and specificity of miRNA-21 in the diagnosis of gastric cancer were 74.36% and 68.18%, respectively, and they were 79.49% and 60.90% for miRNA-335-5p, respectively. There was a negative linear correlation between miRNA-21 and pepsinogen I and gastrin-17 levels ( r = -0.82, -0.74), but there was a positive linear correlation between miRNA-21 and pepsinogen II levels ( r = 0.76). There was a positive linear correlation between miRNA-335-5p and pepsinogen I and gastrin-17 ( r = 0.79, 0.72), but there was a negative linear correlation between miRNA-335-5p and pepsinogen II levels ( r = -0.70). Conclusion:miRNA-21 is highly expressed in patients with gastric cancer, while miRNA-335-5p is lowly expressed. miRNA-21 and miRNA-335-5p are highly correlated with pepsinogen and gastrin-17 levels. miRNA-21 and miRNA-335-5p can be used as effective indices for diagnosis of gastric cancer. Findings of this study are highly innovative and scientific.
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Objective]To investigate the influence of induced before or after the expected date of childbirth on maternal and neonatal outcome in patients with gestational diabetes mellitus which blood glucose well controlled.[Methods]We retrospectively analyzed 238 cases with mild gestational diabetes mellitus who had delivered in this hospital. Mild gestational diabetes mellitus cases were those who only need diet control,exercise therapy,no drug treatment. There were 120 cases who induced in 40 ~ 40+6 weeks was the research group,and 118 cases who induced in 39~39+6 weeks was the control group.[Results]The cesarean section rate be?tween the two groups was no difference(49.2%vs 55.9%,P=0.528);Postpartum hemorrhage rate of the two groups was no differ?ence(10.0%vs14.4%,P=0.299)Birth weight between the two groups was no difference(3.26 ± 0.33)kg vs(3.22 ± 0.34)kg,P =0.448). The incidences of the two groups including fetal distress,large for gestational age infants,neonatal pathological jaundice, neonatal hypoglycemia were no difference(P > 0.05).[Conclusion]Pregnant women with mild gestation diabetes mellitus induced before after 40 completed gestation weeks did not increase cesarean section rate. Pregnancy outcome between the two groups were no difference.It would be better to select the appropriate induction time according to the patient′s condition.
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Objective To determine the effects of adiponectin on high glucose induced BeWo cell proliferation in vitro. Methods BeWo cells were seeded in 96-well plates at the appropriate density. After treatments with high glucose (25 mmol/L), western blot analysis of cyclin D1 and a colorimetric assay (cell counting kit-8, CCK-8) were used to analyse BeWo cells′proliferation, and western blot was used to detect the expression of adiponectin. Moreover, we added adiponectin (20μg/ml) in the culture medium and three methods were utilized for cell proliferation analysis: CCK-8, cell cycle analysis (by flow cytometry) and proliferating cell nuclear antigen (PCNA) immunocytochemical staining. Results Compared to BeWo cells cultured by normal glucose and high mannitol, the proliferation of BeWo cells treated by high glucose increased (P<0.05). Compared with BeWo cells cultured by high mannitol, the expression of adiponectin in BeWo cells treated by high glucose decreased. After added adiponectin in the culture medium, the proliferation of BeWo cells treated by adiponectin+high glucose decreased than that of cells treated by high glucose (0.770±0.050 versus 0.990±0.070, P<0.05);the proportion of G2+S phases of BeWo cells treated by adiponectin+high glucose decreased than that of cells treated by high glucose [(40.7±2.1)%versus (44.9± 3.9)%, P<0.05];the rate of PCNA positive cell in BeWo cells treated by adiponectin+high glucose decreased than that of cells treated by high glucose [(28 ± 5)% versus (44 ± 5)%, P<0.05]. Conclusion Adiponectin could inhibit proliferation of high glucose induced BeWo cells in vitro.
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ObjectiveTo investigate the effect of milk and milk products on morphological structure and epidermal growth factor (EGF) of non-steroidal anti-inflammatory drugs (NSAIDs) induced small intestinal damage in animals.Methods Eighty male SD rats were randomly divided into 5 groups:control group,diclofenac group,diclofenac with 10% low fat milk group,diclofenac with 10% colostrum group and diclofenac with yoghurt group.The animals with milk or colostrum or yoghurt were fed for 5 days before the administration of diclofenac with 15 mg/kg by gavage,once.Then they were observed the scores of anatomical lesion and the scores of tissue damage of mucous membrane and the height of villous at the 24th and 48th hour after making the models.Observation of the change of ultrastructural organization of mucous membrane was carried out with transmission and scanning electron microscope and immunohistocbemistry of EGF.Results The scores of anatomical lesion and tissue damage of mucous membrane of the colostrum group were lower than those of the diclofenac group ( P ＜ 0.05 ).The heights of the pile on small intestine of the24th and 48th hour of the colostrum group were (145.7 ± 16.5) μm and (139.2 ± 19.0) μm,respectively.They were higher than those of the diclofenac group[( 119.2 ± 19.2 ) μm and ( 105.4 ± 18.4 )μm,P ＜ 0.05].However there was no difference of the scores and the height among diclofenac group,milk group and yoghurt group.TEM and SEM of tissues showed that the cytoplasmic membrane and other cellular components of villous epithelial cells were well preserved in colostrum group,and the microvilli in the milk group and yoghurt group were ablated more obviously.The positive area of EGF of small intestine [(6170.5 ± 1483.9) μm2]were higher 48 h after administration of diclofenac compared with the diclofenac group ( P ＜ 0.05 ).The expression of EGF in milk and yoghurt group were no significant statistical difference with the diclofenac group.ConclusionBovine colostrum may have a beneficial effect in prevention of NSAIDs induced small intestinal injuries and preserve mechanical barrier of small intestinal mucosa which is probably relative to EGF.
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Objective To explore the effect of corticotropin releasing factor (CRF) and its receptor on visceral sensitivity and colon motility of irritable bowel syndrome (IBS) rats. Methods sixty SD rats were divided randomly and equally into control group (without treatment),model group (sensitized in turn with camphor odor as conditional stimulation and physical restraint in combination with rectal distention pressure as non-conditional stimulation),treatment control group (injected physiological saline into lateral ventricles before treatment),treatment group 1 (injected CRF-R1antagonist into lateral ventricles before treatment),treatment group 2 (injected CRF-R2 agonist into lateral ventricles before treatment). Then the rats' visceral sensitivity were assessed by AWR,and colonic electricity activities such as volatility,maximum amplitude of fast wave and slow wave,interdigestive number of contraction wave and index of contraction were recorded. The data was analyzed with SPSS 16. 0 software. Results By the amount of ractal water injection to reach AWR=3 as the evaluation index,model group [(0. 90±0. 11) ml] showed higher visceral sensitivity than that of control group [(1. 23±0. 07) ml,F=82. 586,P＜0. 01],and colonic electricity activity increased (P＜0. 05),model was successfully set up. There was no significant difference of the amount of ractal water injection between model group [(0. 90±0. 11) ml] and treatment control group [(0. 81±0. 11) ml,F=3. 734,P＞0. 05]. Compared with treatment control group,the visceral sensitivity decreased in treatment group 1 [(1. 28±0. 07) ml,F=161. 878,P＜0. 01] and treatment group 2 [(1. 22±0.05) ml,F=121. 564,P＜0. 01]. There was no significant difference between treatment control group and model group in electricity activities such as volatility,maximum amplitude of fast wave and slow wave,interdigestive number of contraction wave and index of contraction (all P＞0. 05). While the electricity activities was weakened in treatment group 1 and 2 compared with the treatment control group (all P＜0. 05). Conclusions CRF plays an important role in the pathogenesis of IBS. Inhibition of CRF-R1 or activation of CRF-R2 may lower visceral hypersensitivity and decrease colon motility of rats.
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ObjectiveTo explore the protective effects and possible mechanism of different type of proton pump inhibitors (PPIs) in non-steroid anti-inflammatory drugs (NSAIDs)induced small intestinal injury.MethodsSeventy two SD rats were randomly and equally divided into control group,model group,Omeprazole treated group,Esomeprazole treated group,Rabeprazole treated group and Lansoprazole treated group.Except control group,rats of other groups were gavaged with diclofenac 7.5 mg · kg-1 · d-1,once daily to make NSAIDs related small intestinal injury model.The treated groups were gavaged with Omeprazole 30 mg · kg1· d-1,Esomeprazole 30 mg· kg1 · d-l,Lansoprazole 45 mg · kg1 · d-1 and Rabeprazole 15 mg · kg-1 · d-1 once daily respectively.Continuous administration for five days and then executed,small intestinal tissues were taken and observed for gross and pathological changes.The expression level of nuclear factor erythroid-2-related factor 2(Nrf2) at protein and mRNA level were detected with western blot and real time PCR assay.The qualitative and location of Nrf2 in small intestinal tissue were analyzed by immunohistochemistry staining and the activity of superoxide dismutase (SOD) and malondialdehyde (MDA) in small intestinal tissue were determined with xanthine oxidase method and TBA respectively.ResultsThe successful rate of modeling experiment was 100％.The survival ratio of control group rats,model group,Omeprazole treated group,Esomeprazole treated group,Rabeprazole treated group and Lansoprazole treated group was 12/12,3/12,2/12,1/12,1/12 and 2/12 respectively.The tissue injure scores of Esomeprazole treated group,Rabeprazole treated group and Lansoprazole treated group were significantly lower than that of model group (P＜0.05).The activity of SOD in small intestinal of Rabeprazole treated group was obviously higher than that of model group (P＜ 0.05),while the activity of MDA in Rabeprazole and Esomeprazole treated groups were significantly lower than that of model group (P＜0.05).The results of westen blot indicated that the expression of Nrf2in small intestinal tissue was obviously higher in Rabeprazole treated group than in model group (P＜0.05).The real time PCR results suggested that the expression of Nrf2 at mRNA level in small intestinal tissue of Rabeprazole treated group was obviously higher than those of model and control groups (P＜0.05).Conclusions The protection effects of various PPIs are different in NSAIDs related intestinal injury.There is no obvious protection effect of Omeprazole.Rabeprazole may prevent NSAIDs related intestinal injury by up-regulating expression of Nrf2 and promoting its activation.
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Objective:To explore the protective effect of biochanin A(Bioch A) on lipopolysaccharide(LPS) -induced dopaminergic neurodegeneration. Method:An in vitro model of LPS-induced dopaminergic neurodegeneration was used to investigate the protective effect of Bioch A on dopaminergic neurons against LPS-induced neurotoxicity by measuring [3H] DA uptake and counting TH-immunoreactive cells. Microglia were visualized by staining for the CR3 complement receptor with monoclonal antibody OX-42. The production of nitric oxide(NO) was determined by measuring the accumulated levels of nitrite in the culture supernatant with the Griess reagent,and release of tumor necrosis factor-?(TNF-?) was measured by immunosorbent assay. The production of superoxide was determined by measuring the superoxide dismutase(SOD) -inhibitable reduction of cytochrome C. Results:BiochA dose-dependently attenuated LPS-induced decrease in dopamine(DA) uptake and the number of dopaminergic neurons in rat mesencephalic neuron-glia cultures. BiochA also significantly inhibited LPS-induced activation of microglia and production of TNF-?,NO and superoxide in rat mesencephalic neuron-glia cultures and microglia-enriched cultures. Conclusion:Biochanin A may protect dopaminergic neurons from LPS-induced injury and its effectiveness in inhibiting microglia activation may underlie one of the mechanisms.