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1.
Chongqing Medicine ; (36): 1322-1324, 2015.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-464714

RESUMO

Objective To investigate the effects of miR-200c on proliferation and apoptosis of tongue squamous cell carcino-ma (TCCS)Tca8113 cells.Methods The mimics of miR-200c were transfected into Tca8113 cells using liposome.The Tca8113 cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)assay.The flow cytometry as-say was used to determine the cell cycle and the apoptosis rate of Tca8113 cell.The protein expression levels of Bcl-2 and Caspase-3 in Tca8113 cell was detected by Western-blot.Results The 20,40,80 nmol/L miR-200c mimics groups inhibited the growth of Tca8113 cells,the difference compared with the control group showing statistical significance(P <0.05).The greater the miR-200c mimics concentration and the longer duration of action,the more significant the inhibition effect(P <0.05).After 48h transfecting by miR-200c mimics,the Tca8113 cells were arrested in the G0/G1 phases of cell cycle,and the apoptosis rate of the miR-200c mim-ics groups was significantly increased,the difference compared with the control group showing statistical significance(P <0.05);Western blot verified that the expression amount of Bcl-2 protein in the 20,40,80 nmol/L miR-200c groups was significantly lower than that in the control group,while the expression amount of Caspase-3 protein was significantly higher than that in the control group(P <0.05).Conclusion The overexpression of miR-200c might inhibit the proliferation of Tca8113 cell and induces their ap-optosis.

2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-403523

RESUMO

BACKGROUND: In many studies, rats were commonly used as models of retrorsine-induced hepatic injury. Some reports have confirmed that retrorsine cannot inhibit proliferation of mouse hepatic cells. Other reports have shown that retrorsine has inhibitory effects on proliferation of mouse hepatic cells. OBJECTIVE: To study the liver regeneration after hepatic injury by creating mouse models treated with partial hepatectomy combination with retrorsine. METHODS: A total of 40 C57BL/6J mice were equally and randomly assigned to 2 groups. In the partial hepatectomy combined with retrorsine group, intraperitoneal injection of retrorsine 70 mg/kg was conducted, twice, within an interval of 2 weeks. Four weeks later, 2/3 hepatectomy was performed. In the partial hepatectomy group, intraperitoneal injection of saline 70 mg/kg was performed, twice, with an interval of 2 weeks. Four weeks later, 2/3 hepatectomy was performed. At 14 days after partial hepatectomy, the restoration of the livers was observed. The liver cell injury was observed at 3, 7 days with hematoxylin-eosin staining. The hepatocyte proliferation was observed at 3 days with BrdU staining. Oval cell proliferation was observed at 3, 7and 14 days with CK19 and C-kit antibody immunohistochemistry.RESULTS AND CONCLUSION: In the partial hepatectomy group, the damaged liver nearly restored to normal at 14 days after partial hepatectomy, and the result was contrary to partial hepatectomy combined with retrorsine group. Hematoxylin-eosin staining demonstrated that significant degeneration changes in hepatic cells in the partial hepatectomy combined with retrorsine group. BrdU staining showed that hepatocyte proliferation at day 3 was significantly determined in the partial hepatectomy group, but few in the partial hepatectomy combined with retrorsine group. CK19 and C-kit immunohistochemistry demonstrated that visible oval cell proliferation was seen in mice of partial hepatectomy combined with retrorsine group. First of all, hepatic oval cells appeared in portal area and differentiated into hepatic cells and bile duct cells, and then grew into the hepatic lobule gradually. These indicated that retrorsine can obviously inhibit hepatocyte regeneration after liver injury in mice. The model of mice treated with retrorsine and partial hepatectomy could induce oval cell proliferation.

3.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-391687

RESUMO

Objective To investigate the occurrence of apoptosis and its relationship with endocrine hormones altemtions in rats with acute obstructive pancreatitis(AOP). Methods The model of AOP wag establisbed by ligation of pancreaticobiliary duct.8,12 hrs after operation,the serum insulin,glucagons and amvlase were determined;pancreatic tissues were harvested and apoptotic rate wag evaluated by TUNEL and flow cytometry(Annexin V-FITC/PI assay).Results 8 and 12 hrs after AOP induction,serum amylase levels wefe(1198±687)U/L and(1698±1103)U/L respectively;serum insulin levels were(8.1±5.8)ng/ml and (12.7 ±6.9)ng/ml respectively;sertlm glucagon levels were(6.8±4.6)ng/ml and(7.3±2.9)ng/ml respectively;all these parameters were significantly high than(404±222)U/L,(5.6±2.7)ng/ml and(2.6±2.1)ng/ml in the sham operation group(P<0.05).AnnemnV FITC/PI assay confirmed apoptosis occurred both in exocrine acinus cells and endocrine panclreas islet;and the apoptotic rate wag(20.5±11.2)%and (15.5±8.9)%at 8 and 12 hrs after AOP induction,which wag significantly high than(4.2±1.6)%in the sham operation group(P<0.05).Conclusions Cell apoptosis occurred in both acinar and islet in the model of AOP,and this may be the pathophysiological basis of endocnne hormones alterations in the model of AOP.

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