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Yan Y.,Peking University | Li G.,Peoples Liberation Army 202 Hospital | Tian X.,Dalian Medical University | Ye Y.,Peking University | And 4 more authors.
International Journal of Molecular Medicine | Year: 2015

Ischemic preconditioning (IPC) ameliorates ischemia/reperfusion (I/R) injury in a number of organs, and the glycogen synthase kinase-3β (GSK-3β)/β-catenin signaling pathway regulates I/R-induced proliferation and apoptosis in the central nervous system and heart. However, the function of this signaling pathway in IPC during liver I/R remains unclear. Thus, in this study, we aimed to investigte the role of the GSK-3β/β-catenin pathway during I/R and following ischemic preconditioning. For this purpose, 30 Sprague-Dawley rats were randomly divided into the sham-operated, the I/R and the IPC groups (n=10). Following reperfusion, liver pathology, as well as alanine aminotransferase (ALT), aspartate aminotransferase (AST), maleic dialdehyde (MDA) and superoxide dismutase (SOD) levels were assessed. Western blot analysis was performed to quantify the GSK-3β, Ser9-phospho-GSK-3β (p-GSK-3β), cytosolic and nuclear β-catenin, vascular endothelial growth factor (VEGF), Bcl-2 and survivin levels. In addition, the Bcl-2 and survivin mRNA levels were assessed by RT-qPCR. Compared with the sham-operated group, I/R increased serum ALT, AST and MDA activity and decreased SOD levels, while IPC significantly decreased serum ALT, AST and MDA activity and increased SOD levels, compared with the I/R group. Simultaneously, I/R increased p-GSK-3β protein expression, and decreased Bcl-2 and survivin protein and mRNA levels. IPC further increased the protein expression of p-GSK-3β, and also increased cytosolic and nuclear β-catenin and VEGF expression compared with the I/R group; the expression of Bcl-2 and survivin was also increased by IPC, both at the mRNA and protein level. The total GSK-3β expression remained unaltered in all the groups. In conclusion, our data demonstrate that IPC exerts protective effects against liver injury induced by I/R and activates the GSK-3β/β-catenin signaling pathway.


PubMed | Peoples Liberation Army 202 Hospital, Peking University and Dalian Medical University
Type: Journal Article | Journal: International journal of molecular medicine | Year: 2015

Ischemic preconditioning (IPC) ameliorates ischemia/reperfusion (I/R) injury in a number of organs, and the glycogen synthase kinase-3 (GSK-3)/-catenin signaling pathway regulates I/R-induced proliferation and apoptosis in the central nervous system and heart. However, the function of this signaling pathway in IPC during liver I/R remains unclear. Thus, in this study, we aimed to investigte the role of the GSK-3/-catenin pathway during I/R and following ischemic preconditioning. For this purpose, 30 Sprague-Dawley rats were randomly divided into the sham-operated, the I/R and the IPC groups (n=10). Following reperfusion, liver pathology, as well as alanine aminotransferase (ALT), aspartate aminotransferase (AST), maleic dialdehyde (MDA) and superoxide dismutase (SOD) levels were assessed. Western blot analysis was performed to quantify the GSK-3, Ser9-phospho-GSK-3 (p-GSK-3), cytosolic and nuclear -catenin, vascular endothelial growth factor (VEGF), Bcl-2 and survivin levels. In addition, the Bcl-2 and survivin mRNA levels were assessed by RT-qPCR. Compared with the sham-operated group, I/R increased serum ALT, AST and MDA activity and decreased SOD levels, while IPC significantly decreased serum ALT, AST and MDA activity and increased SOD levels, compared with the I/R group. Simultaneously, I/R increased p-GSK-3 protein expression, and decreased Bcl-2 and survivin protein and mRNA levels. IPC further increased the protein expression of p-GSK-3, and also increased cytosolic and nuclear -catenin and VEGF expression compared with the I/R group; the expression of Bcl-2 and survivin was also increased by IPC, both at the mRNA and protein level. The total GSK-3 expression remained unaltered in all the groups. In conclusion, our data demonstrate that IPC exerts protective effects against liver injury induced by I/R and activates the GSK-3/-catenin signaling pathway.


Gong Y.-H.,Peoples Liberation Army 202 Hospital | Jin H.-T.,Peoples Liberation Army 202 Hospital
Journal of Dalian Medical University | Year: 2014

Objective: To measure the treatment effect of rotary gamma knife on intracranial arteriovenous malformation (AVM).Methods: Treat 59 case AVM with Chun Rui FreeGS-A rotary gamma knife.Results: The examination MRI or DSA showed that AVM completely closed in 41 cases. Most casesfound cure or relief in their clinical symptoms.Conclusion: Gamma Knife is a safe and effective method for the treatment AVM.


Chen R.-L.,Dalian Medical University | Piao F.-Y.,Dalian Medical University | Li S.-Y.,Dalian Medical University | Wang Z.-M.,Dalian Medical University | And 4 more authors.
Journal of Dalian Medical University | Year: 2014

Objective: To investigate the method of isolation, cultivation and CFSE label of rat bone marrow mesenchymal stem cells (BMSCs).Methods: BMSCs were isolated and expansion by adherent method. The specific surface markers of fifth generation BMSCs; CD29, positive rate was 90. 10%. CD90, positive rate was 96.61%. CD45, negative rate was 0.40%, via flow cytometry, and differentiation. BMSCs labeled with CFSE were observed under fluorescence microscope and the labeling efficiencies were assessed. The effect of CFSE on the survival of BMSCS were tested by trypanblue.Results: FCM detected that CD29 and CD90 were positively expressed, but CD34 was negatively expressed in BMSCs. Following induction, oil red O staining and alizarin red staining produced a strong reaction in cells. Nearly 100 % BMSCs were CFSE - labeled when BMSCs reacted with 10 μmol/L CFSE for 15 min. At the same time, the highest viability of BMSCs were observed(P >0.05).Conclusion: BMSCs were obtained by adherent method. And staining with CFSE at 10 μmol/L for 15 min was the optimal condition for rat BMSCs labeling in vitro.


Jin H.-T.,Peoples Liberation Army 202 Hospital | Piao F.-Y.,Dalian Medical University | Guan H.,No 210 Hospital Of Pla | Li S.-Y.,Dalian Medical University
Journal of Dalian Medical University | Year: 2015

Objective: To observe the effect of acrylamide on the neurobehavioral and neurophysiology of rats. Methods: Thirty rats were randomly and evenly divided into 3 groups: control group, low - and high - dose group. The rats in 3 groups were injected intraperitoneally with normal saline, 20 mg/kg and 40 mg/kg acrylamide respectively for 10 weeks (3 d/w). The general state, gait and weight changes of the rats were observed, and nerve conduction velocity and distal latency were detected. Results: Compared with the control group, the weight of rats exposed to acrylamide decreased progressively with prolonged exposure. After 8 weeks, there was weight loss in the rats of high - dose group. In rats of low - and high - dose group, abnormal gait were found on 8 w and 4 w respectively and the gait scores were 2.00 ±0.00 and 4.00 ± 0.00 respectively at 10 weeks. From the 3rd week, distal latency increased and nerve conduction velocity decreased significantly. Compared with the control group, nerve conduction velocity were increased by 15.13% and 33.06%, and distal latency decreased by 17.41% and 58. 75% in the low - and high - dose groups (P < 0. 05). Conclusion: The chronic exposure to acrylamide would cause the abnormal changes of neurobehavioral and neurophysiological in rats, then lead to peripheral neuropathy.

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