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Objective: To investigate the effects and mechanism of microRNA ( miR-130a) on proliferation and apoptosis of pancreatic cancer cells by targeting FOS-like antigen 1 (FOSLl). Methods: Pancreatic cancer cells PANC-1 were routinely cultured and divided into the NC group and miR-130a mimic group. Cells in the NC group were transfected with control, miR-130a mimic group with miR-130a simulant by Liposome 2000. CCK-8 was used to detect the proliferation activity of cells. Flow cytometry was used to detect the apoptosis of cells. Targetscan7. 1 prediction software and dual luciferase reporter gene test were used to detect miR-130a targeted-regulating FOSLl gene. The FOSLl overexpression plasmid was constructed, and co-transfected into PANC-1 cells with miR-130a, and then PANC-1 cells were divided into the NC group, miR-130a mimic group, and miR-130a mimic + oe-FOSLl group. Cells in the NC group were transfected with control, miR-130a mimic group with miR-130a mimic, and the miR-130a mimic + oe-FOSLl group with miR-130a mimic and FOSLl overexpression plasmid. Western blotting was used to detect the expression of p53 protein in each group. Results: Compared with the NC group, the proliferation ab山ty of PANC-1 cells in the miR-130a mimic group decreased (P < 0. 05), and apoptosis increased (P < 0. 05). The double luciferase reporter gene test coufirmed that FOSLl was a target gene of miR-130a. Compared with the NC group, the proliferation ability of PANC-1 cells in miR-130a mimic group and the miR-130a mimic + oe-FOSLl group decreased, and apoptosis increased (both P < 0. 05). Compared with the miR 130a mimic group, the proliferation ability of PANC-1 cells in the miR-130a mimic + oe-FOSLl group increased, and apoptosis decreased (both P < 0. 05). Compared with the NC group, the expression of FOSLl protein in the miR-130a mimic group and miR-130a mimic + oe-FOSLl group decreased and p53 protein increased ( both P < 0. 05 ). Compared with the miR-130a mimic group, the expression of FOSLl protein in the miR-130a mimic + oe-FOSLl group increased and p53 protein expression decreased ( both P < 0. 05 ). Conclusion: MiR-130a targeting FOSLl can inhibit the proliferation of pancreatic cancer cells and promote apoptosis by up-regulating the expression of p53. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of leonurine( LEO) on the cerebral ischemia-reperfusion injury mice and its mechanism. Methods Totally 120 healthy male Kunming mice were randomly divided into three groups: the sham group,the model group,and the LEO group,with 40 mice in each group. The cerebral ischemia reperfusion models were established by the middle cerebral artery occlusion method in mice of all groups except the sham group. The mice in the sham operation group were operated in the same method except that the suture was not inserted. At 30 minutes after model establishment,the mice in the LEO group was intraperitoneally injected with LEO 15 mg/( kg·d). The mice in the sham group and the model group received the same volume of normal saline. At 24 h after model establishment,the brain tissues of the infarction site were taken and the volume of cerebral infarction was measured by TTC staining. The brain water content was weighed to evaluate the degree of brain edema. The blood-brain barrier permeability was measured by Evans blue( EB) method. The morphology of brain tissue was observed by HE staining. The expression of p-p38 and tight junction protein( ZO-1) protein in the brain tissues was detected by Western blotting. The expression of inflammatory factors including IL-1β,IL-6 and tumor necrosis factor-α( TNF-α) mRNA was detected by RT-PCR. Results The cerebral infarction volume ratio,brain water content,and EB content in the model group were higher than those in the sham operation group and were lower than those in the model group( all P < 0. 05). In the model group,a large number of neurons showed pathological changes of ischemic anoxic necrosis. However,compared with the model group,the pathological changes of brain tissues in the LEO group were significantly improved. The expression of p-p38 protein was higher and the expression of ZO-1 protein was lower in the model group than that in the sham group. The expression of p-p38 protein was lower and the expression of ZO-1 protein was higher in the LEO group than that in the model group( P < 0. 05). The expression levels of IL-1β,IL-6,and TNF-α mRNA were higher in the model group than those in the sham group. The expression levels of IL-1β,IL-6 and TNF-α mRNA were lower in the LEO group than those in the model group( all P < 0. 05). Conclusion LEO can improve the nerve damage and alleviate the permeability of blood-brain barrier in mice with ischemia-reperfusion.The mechanism may be related to the inhibition of p38 MAPK signaling pathway and reduction of the inflammatory response. [ABSTRACT FROM AUTHOR]

Objective To investigate the changes in levels of portal venous blood prostacyclin I2 ( PGI2) and thromboxane A2 (TXA2) in patients with colorectal carcinoma and their clinical significance. Methods Sixty patients with colorectal carcinoma were selected in the study，including 22 cases with synchronous liver metastasis ( liver metastasis group )，38 cases without liver metastasis ( non-liver metastasis group )，20 cases in stage II of pTNM staging，32 cases in stage H ，and 8 cases in stage IV. Meanwhile，16 cases of postoperative adhesive intestinal obstruction were considered as controls ( control group ). The levels of PGI2 and TXA2 in the portal venous blood，tumor tissues，and normal colorectal mucosae were detected by radioimmunoassay，respectively ，and then were compared with those of the controls. Results Compared with the normal colorectal mucosae，the level of TXA2 increased，while the level of PGI2 decreased significantly in the colorectal cancer tissues ( both P < 0 .01 ); compared with the control group，the level of PGI2 increased，and the ratio of PGI2/TXA2 and TXA2 decreased significantly in the non-liver metastasis group and liver metastasis group ( all P < 0. 01 ). Compared with the non-liver metastasis group， the level of portal venous blood PGI2 and the ratio of PGI2/TXA2 decreased，TXA2 increased in the liver metastasis group (all P < 0.01). Compared with patients whose tumor maximum diameter ≤3.0 cm，3. 1 cm - 4 . 0 cm，the level of PGI2 and the ratio of PGI2/TXA2 decreased，TXA2 increased in patients with tumor diameter > 4 .0 cm ( all P < 0.05 ). The ratio of PGI2/TXA2 value of portal vein was negatively correlated with the size of the tumor ( r = -0 .770 ). The ratio of PGI2/TXA2 in portal vein blood of patients with colorectal cancer and synchronous liver metastasis was lower than that without metastasis ( P < 0 .01 ). Conclusions The level of TXA2 increases and the ratio of PGI2/TXA2 decreases in the portal vein blood of patients with colorectal cancer. The decreased ratio of PGI2/TXA2 of portal vein blood may be one of the important causes of synchronous liver metastasis of colorectal cancer. [ABSTRACT FROM AUTHOR]