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Objective@#To investigate the expression of integrin α5 in cervical cancer, and to explore its relationship with clinicopathological characteristics of patients with cervical cancer.@*Methods@#Immunohistochemistry was used to detect the expression of integrin α 5 in cervical cancer tissues of 60 cases and normal cervical paraffin-embeded tissues of 20 cases of benign uterine lesions undergoing hysterectomy from Qingdao Municipal Hospital between January 2014 and December 2017. Real-time quantitative polymerase chain reaction (RT-PCR) was used to detect the mRNA expression level of integrin α5 in 20 fresh cervical cancer tissues and 20 normal cervical tissues collected from benign cervical lesions in Qingdao Municipal Hospital between January 2018 and July 2018. The relationship between the expression of integrin α5 and the clinicopathological characteristics of patients with cervical cancer was analyzed.@*Results@#The positive expression rate of integrin α5 protein in cervical cancer and normal cervical tissues was 63.3% (38/60), 35.0% (7/20), respectively, and the difference was statistically significant (χ 2 = 4.893, P < 0.05). The expression of integrin α5 mRNA in cervical cancer was 1.6±0.4 times as high as that in normal cervical tissues (t = 5.529, P < 0.01). The positive expression of integrin α5 protein was associated with lymph node metastasis in cervical cancer patients (Z = -2.636, P = 0.008).@*Conclusion@#The high expression of integrin α5 is related to lymph node metastasis of cervical cancer, and integrin α5 may be a new potential target for treatment of cervical cancer.
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Objective To investigate the expression of integrin α5 in cervical cancer, and to explore its relationship with clinicopathological characteristics of patients with cervical cancer. Methods Immunohistochemistry was used to detect the expression of integrin α 5 in cervical cancer tissues of 60 cases and normal cervical paraffin-embeded tissues of 20 cases of benign uterine lesions undergoing hysterectomy from Qingdao Municipal Hospital between January 2014 and December 2017. Real-time quantitative polymerase chain reaction (RT-PCR) was used to detect the mRNA expression level of integrin α5 in 20 fresh cervical cancer tissues and 20 normal cervical tissues collected from benign cervical lesions in Qingdao Municipal Hospital between January 2018 and July 2018. The relationship between the expression of integrinα5 and the clinicopathological characteristics of patients with cervical cancer was analyzed. Results The positive expression rate of integrin α5 protein in cervical cancer and normal cervical tissues was 63.3％(38/60), 35.0％(7/20), respectively, and the difference was statistically significant (χ2=4.893, P<0.05). The expression of integrin α5 mRNA in cervical cancer was 1.6 ±0.4 times as high as that in normal cervical tissues (t= 5.529, P< 0.01). The positive expression of integrin α5 protein was associated with lymph node metastasis in cervical cancer patients (Z= -2.636, P= 0.008). Conclusion The high expression of integrinα5 is related to lymph node metastasis of cervical cancer, and integrin α5 may be a new potential target for treatment of cervical cancer.
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BACKGROUND: Mesenchymal stem cells can protect and repair the liver of rats with liver failure, but the mechanisms are not completely clear. OBJECTIVE: To explore the protective effects and related mechanisms of intravenous injection of human adipose-derived mesenchymal stem cells on acute liver failure in rats. METHODS: Thirty-six Sprague-Dawley rats (provided by Qingdao Daren Fucheng Animal Husbandry Co., Ltd. in China) were randomly divided into control group, model group and transplantation group. Animal models of acute liver failure were established by intraperitoneal injection of D-galactosamine in the model group and the transplantation group. One day after modeling, the rats in the transplantation group were injected with human adipose-derived mesenchymal stem cell suspension, and those in the model group were injected with the same amount of saline. After 1 and 3 days of cell transplantation, the serum levels of alanine aminotransferase, aspartate aminotransferase, and total bilirubin were measured. Three days after cell transplantation, the serum levels of tumor necrosis factor-α, interleukin-6 and interleukin-10 were detected, the pathological changes of the rat liver were observed by hematoxylin-eosin staining, and the activity of glycogen synthase kinase-3β protein in the liver tissue was detected by western blot. RESULTS AND CONCLUSION: Compared with the model group, there was a significant reduction in the serum levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin, tumor necrosis factor-α, interleukin-6 and interleukin-10 in the transplantation group (P < 0.05). Inflammation and necrosis of liver tissues in the transplant group were alleviated compared with the model group. The activity of glycogen synthase kinase 3β in the liver tissue of the transplanted group was lower than that of the model group (P < 0.05). Overall, these results indicate that human adipose-derived mesenchymal stem cells can alleviate hepatic inflammation and pathological injury, and improve the liver function in rats with acute hepatic failure. Moreover, the mechanism may be related to the inhibition of glycogen synthase kinase 3β activity.
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BACKGROUND: Mesenchymal stem cells can protect and repair the liver of rats with liver failure, but the mechanisms are not completely clear. OBJECTIVE: To explore the protective effects and related mechanisms of intravenous injection of human adipose-derived mesenchymal stem cells on acute liver failure in rats. METHODS: Thirty-six Sprague-Dawley rats (provided by Qingdao Daren Fucheng Animal Husbandry Co., Ltd. in China) were randomly divided into control group, model group and transplantation group. Animal models of acute liver failure were established by intraperitoneal injection of D-galactosamine in the model group and the transplantation group. One day after modeling, the rats in the transplantation group were injected with human adipose-derived mesenchymal stem cell suspension, and those in the model group were injected with the same amount of saline. After 1 and 3 days of cell transplantation, the serum levels of alanine aminotransferase, aspartate aminotransferase, and total bilirubin were measured. Three days after cell transplantation, the serum levels of tumor necrosis factor-α, interleukin-6 and interleukin-10 were detected, the pathological changes of the rat liver were observed by hematoxylin-eosin staining, and the activity of glycogen synthase kinase-3β protein in the liver tissue was detected by western blot. RESULTS AND CONCLUSION: Compared with the model group, there was a significant reduction in the serum levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin, tumor necrosis factor-α, interleukin-6 and interleukin-10 in the transplantation group (P < 0.05). Inflammation and necrosis of liver tissues in the transplant group were alleviated compared with the model group. The activity of glycogen synthase kinase 3β in the liver tissue of the transplanted group was lower than that of the model group (P < 0.05). Overall, these results indicate that human adipose-derived mesenchymal stem cells can alleviate hepatic inflammation and pathological injury, and improve the liver function in rats with acute hepatic failure. Moreover, the mechanism may be related to the inhibition of glycogen synthase kinase 3β activity.
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Objective To investigate the effect of Irisin on proliferation,apoptosis,migration and invasion of human cholangiocarcinoma cell line Hucct-1.Methods After treatment with Irisin,CCK-8 assay and flow cytometry assay were conducted to investigate the effect of Irisin on proliferation and apoptosis of cholangiocarcinoma cells.Scratch test and transwell invasion assay were used to studythe effect of Irisin on the migration and invasion ability of cholangiocarcinoma cells.Western blot was utilized to detect the expression of E-cadherin,N-cadherin and Vimentin in cholangiocarcinoma cells.Results CCK-8 assay showed that Irisin inhibited cholangiocarcinoma cell proliferationin a dose-dependent manner.Flow cytometry assay showed that the apoptosis rate of Irisin group [(14.8 ±0.9)％] was higher than that in the control group [(5.4±0.6)％],(P＜0.05).The scratch test showed that the rate of cell scratch healing in Irisin group [(15.0± 1.0)％] was significantly lower than that in the control group [(28.0±2.0)％] (P＜0.05).Transwell invasion test showed that the number of cells in Irisin group was (96.0±7.0),which was significantly lower than that in control group (155.0± 9.0) (P＜0.05).Western blot showed that the expression of E-cadherin increased and N-cadherin and Vimentin decreased after Irisin treatment.Conclusion Irisin inhibits proliferation,migration and invasion and promote apoptosis of cholangiocarcinoma cells.
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Objective To observe the effect of human adipose mesenchymal stem cells (hADMSCs) on pancreatic tissue repair and inflammatory reaction of acute necrotic pancreatitis (ANP) in rat, and explore the possible mechanism.Methods Isolation and purification of hADMSCs and flow cytometry to detect the the surface markers including CD90, CD29, CD34 and CD45 were performed.Eighty SD male rats with the body weight of 170~210 g were randomly divided into 4 groups.There were 8 rats in the control group, 24 rats in other group.Control group underwent no treatment;sham operation group underwent intestinal wall stirring and then abdominal closure;ANP model group was established by open abdominal retrograde injection of sodium taurocholate into bile duct;and in hADMSCs group, DAPI labeled hADMSCs were injected by tail vein into the rat at 12 h after sodium taurocholate injection.The survival of the rats, and gross morphological and pathological changes of the pancreas was observed at 12, 24, and 48 h, and the serum TNF-α, IL-6, IL-10 and amylase were detected.The distribution of hADMSCs in the pancreas, liver and lung was examined in hADMSCs group.Results Rats in control group and sham operation group were all alive.In ANP group, 5 and 11 rats were dead at 24 and 48 h, respectively, and in hADMSCs group 12 rats were dead at 48 h.Compared with ANP group, the difference was not statistically significant (P>0.05).The pathological changes of the pancreas were significantly less severe in hADMSCs group than in ANP group.In hADMSCs group, the amylase at 12, 24 and 48 h was(999±110 )、(1 831±110)、(3 991±130 )U/L;TNF-α level was (62.40±2.35), (80.51±4.51) and (93.46±6.60)ng /L;IL-6 was (60.46±7.34), (80.61±8.40) and(100.58±9.49)ng /L;and these were all significantly lower than those in ANP model group [amylase (2 402±146), (3 292±137) and (5 632±112)U/L;TNF-α(87.13±3.39), (105.41±10.06), (114.57±3.06)ng/L;IL-6 (70.67±10.90)、(107.61±10.53)、(145.34±10.48)U/L], and the differences were all statistically significant (all P<0.05).IL-10 in hADMSCs group was (56.63±6.35), (81.32±5.96), (100.26±6.51)ng/L, which were increased compared with those in ANP model group [(45.26±8.04), (68.25±8.42), (80.38±5.71)ng/L], and the difference was statistically significant (all P<0.05).hADMSCs can migrate to the pancreas, liver, lungs and other damaged tissue, with most in pancreatic tissue, less in lung tissue, and least in liver tissue.Conclusions The mechanism of hADMSCs in repairing pancreatic tissue injury was associated with inhibiting TNF-α and IL-6 secreting and increasing IL-10, thus reducing inflammatory reaction.
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BACKGROUND: Adipose-derived mesenchymal stem cells (ADMSCs) can improve the liver function of rats with liver failure, which illustrates the important research value in the field of tissue engineering and cell transplantation.OBJECTIVE: To evaluate the therapeutic potential of human ADMSCs in heart failure rats and to discuss the possible biological mechanisms involved.METHODS: Heart failure rats were randomized into model and ADMSCs groups, which were given normal saline or DAPI-labeled human ADMSCs (3.0×106) via the tail vein. At 1, 3, 7 days after transplantation, we detected the biochemical indexes for liver function in rats. At 3 days after transplantation, the serum levels of cytokines, such as tumor necrosis factor α and interleukin-10, were detected, the histomorphological changes in the liver were observed by hematoxylin-eosin staining, and the protein expression of proliferating cell nuclear antigen was detected by western blot. RESULTS AND CONCLUSION: We found that human ADMSCs could migrate to the liver and lung tissues in rats after the transplantation via the tail vein. At 1 and 3 days after transplantation, the levels of serum alanine aminotransferase and aspartate aminotransferase were significantly reduced in the ADMSCs group as compared with the model group (P< 0.05); furthermore, the secretion of tumor necrosis factor α and interleukin-10 was significantly suppressed at 3 days after cell transplantation (P < 0.05). The results of hematoxylin-eosin staining indicated a significant improvement in liver degeneration and necrosis. The expression of proliferating cell nuclear antigen protein in the ADMSCs group was significantly up-regulated compared with the model group. To conclude, human ADMSCs can inhibit the inflammatory reaction and up-regulate the expression of proliferating cell nuclear antigen, to promote the regeneration of liver cells and he recovery of liver function.
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BACKGROUND:Recent studies have shown that adipose-derivedmesenchymal stem cells (ADMSCs) not only have multilineage differentiation potential, but also exert an important role in blood sugar balance and hormone production.OBJECTIVE:To observe the differentiation potential of human ADMSCs (hADMSCs) into functional islet-like cells and the therapeutic effect of hADMSCs transplantation in diabetic rats.METHODS:PDX-1 gene was transfected into hADMSCs by adenovirus. Cell differentiation and insulin secretion were identified and detected by dithizone staining and ELISA, respectively. Twenty male Sprague-Dawley rats were randomly divided into control group (n=4), diabetes group (n=8) and transplantation group (n=8). Rats in the latter two groups were subjected to making diabetic models by 65 mg/kg streptozotocin injection. Afterwards, rats in the transplantation group were given PDX-1 transfected ADMSCs via the tail vein.RESULTS AND CONCLUSION:At 15 days after transfection, the number of insulin positive cells and insulin secretion were both increased significantly (P < 0.05). Fasting glucose levels in the transplantation group decreased significantly (P < 0.05), while the body weight increased significantly (P < 0.05). In the diabetic group, the fasting glucose level still maintained at a high level, and the body weight of rats was significantly decreased. These results implicated that PDX-1 gene could induce hADMSCs differentiating into functional islet-like cells. PDX-1 transfected ADMSCs transplantation is effective in treating diabetic rats, but the mechanism needs further study.
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[Summary] Berberine is akind of alkaloids extracted from Chinese herb medicine in cludingphellod endron ,coptis and radix berberidis .In recent years ,the pharmacological effects of berberinewas investigated extensively including anti-infection ,anti-arrhythmia ,protection of ischemic myocardium ,anti-hypertension , anti-tumor ,anti-HIV .And there are increasing reports about its hypoglycemic effect ,but its mechanism remains unclear .Here we summarize the possible mechanism of hypoglycemic effect and clinical efficacy of berberine .
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Objective To observe the effects of doxazosin on the expression of type Ⅰ and type Ⅲ collagen fiber in autoantibodies against α1-adrenergic receptors (α1-AA) positive diabetic rats,and to investigate the protective mechanism of doxazosin on cardiomyopathy of diabetic rats.Methods After establishment of diabetes model with streptozocin,diabetic rats were randomly divided into diabetic group (group A,n =10),doxazosin treated group (group B,n =10),α1-AA mediated group (group C,n =8),α1-AA plus doxazosin treated group (group D,n =8).Group C and group D were injected α1-AA (100 μg/100 g) by caudal vein at 0,4,8,12,and 16 weeks.Doxazosin (0.36 mg · kg-1 · d-1) was administered by lavage for 16 weeks in group B and group D,and other groups were given the same volume of saline every day.Expressions of type Ⅰ and type Ⅲ collagen fibers in myocardium of left ventricle were detected by immunohistochemical staining.Pathological changes in the myocardium were observed by both light and electron microscopes.Changes in collagen fiber in myocardium were detected by Van Gieson staining.Results Among various groups,there was no significant difference in blood glucose levels (P ＞ 0.05).After the intervention of doxazosin,body weight in group B and group D was greater than that of group A and group C (P＜0.05 or P＜0.01).Expression of type Ⅰ and type Ⅲ collagen fibers in myocardium in group D was lower than that in group C (P＜0.05).Expression of type Ⅰ and type Ⅲ collagen fibers in group B was lower than that in group A (P＜0.05) as well.Myocardial pathological changes in group C were most serious,showing reduced mitochondrial,vacuolar degeneration,and interstitial collagen hyperplasia.Cardiomyopathy in group D and group B was less marked as compared with that in group C and group A,respectively.Myocardial collagen fiber in group C was significantly increased and showed poor alignment.Compared with group C,myocardial collagen deposition in group D was obviously reduced.Conclusions Doxazosin may suppress type Ⅰ and type Ⅲ collagen expressions in myocardium of α1-AA mediated diabetic rats,resulting in alleviation of myocardial fibrosis and protection of myocardium in diabetic rats.
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To observe the relationship between positive rate of β1-adrenergic and AT1 receptors autoantibodies with serum concentration of cystatin C in 371 patients with diabetic nephropathy patients,107 patients with type 2 diabetes,and 47 subjects as healthy control.In patients with diabetic nephropathy,the positive rates of the β1 and AT1 receptors autoantibodies were significantly higher than those in patients with type 2 diabetes and normal controls.The titers of β1 and AT1 receptors autoantibodies in diabetic nephropathy patients with abnormal cystatin C were significantly higher than those with normal cystatin C concentration.These findings suggested that β1 and AT1 receptors autoantibodie may play important roles in the pathogenesis of diabetic nephropathy.