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Objective To investigate the effects of brain-derived neurotrophic factor (BDNF) pretreatment on H9c2 myocardial hypoxia/reoxygenation (H/R) injury, and explore its mechanism. Methods The H9c2 myocardial cells were cul?tured in vitro and (95%O2+5%CO2) oxygen cultured 12 h after (95%N2+5%CO2) hypoxia cultured 4 h to establish the H/R model. The cells were divided into normal control group, H/R group, different concentrations (1, 10, 100μg/L) BDNF pre?treatment in H/R groups and TrkB-inhibitor group (with 100μg/L BDNF and 1∶1 000 TrkB inhibitor pre-treatment in H/R group). The cell survival rate was measured by MTT method in different groups. The lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA) and superoxide dismutase (SOD) content and activity were detected after H/R injury. The apoptotic rate of H9c2 myocardial cells were detected by flow cytometry, and the expressions of TrkB, Bcl-2 and Bax protein were detected by Western blot assay. Results Compared with the normal control group, the survival rate of H9c2 myocardial cells was decreased significantly in H/R model group (P < 0.05), LDH, CK and MDA contents were increased and SOD activity was decreased (P<0.05). The cell apoptosis rate was increased significantly (P<0.05). The anti-apoptosis Bcl-2 protein expression was decreased, pro-apoptosis Bax protein expression was increased in H/R model group (P<0.05). Compared with the H/R model group, the cell survival rates of H9c2 myocardial cells were increased after pre-treatment with different concentrations of BDNF (P<0.05);LDH, CK and MDA contents were decreased and SOD activity were in?creased respectively (P < 0.05). The cell apoptotic rates were decreased (P < 0.05). The expressions of TrkB receptor and Bcl-2 protein gradually increased, while the expression of Bax protein was gradually decreased (P<0.05). The role of BDNF was inhibited by TrkB inhibitor. Conclusion BDNF pre-treatment can promote the cell survival rate of H9c2 myocardial cells after H/R injury, which plays a protective role by inhibiting the cell apoptotic rate and maintaining antioxidant capacity, and associates with BDNF-TrkB signaling pathways.
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Objective To observe the efficacy and safety of recombinant tissue type plasminogen activa-tor (rt-PA)for the treatment of the patients with wake-up ischemic stroke (WUS)under the guidance of multimode CT. Methods Eighteen patients with WUS (a thrombolytic group)suitable for intravenous thrombolysis after multimode CT imaging screen at the Department of Neurology,Shiyan Hospital of Integrated Traditional and Western Medicine,Hubei Province from October 2012 to October 2014 were enrolled retrospectively. Twenty patients with WUS (a control group)who underwent multimode CT imaging screen were suitable for intravenous thrombolysis,but because of exceeding time window or rejecting thrombolysis and other reasons without having intravenous thrombolysis from February 2012 to February 2014 were enrolled retrospectively. The control group was treated with conventional therapy and the thrombolytic group was treated with rt-PA (0. 9 mg/kg)intravenous thrombolytic therapy. The indicators including fibrinogen (Fib),coagulation function (prothrombin time [PT ]),activated partial thromboplastin time (APTT ), platelet (PLT ),high-sensitivity C-reactive protein (hs-CRP ),National Institute of Health Stroke Scale (NIHSS )scores,and activities of daily living scores (Barthel index)at before treatment and 24 h,7 and 14 days after treatment were observed respectively. The adverse events and complications were documented and compared with the control group. Results There were no significant differences in Fib,PT,APTT, PLT,hs-CRP,NIHSS score and Barthel index before treatment between the thrombolytic group and the con-trol group (all P>0. 05);at day 7 and 14 after treatment in the thrombolytic group,compared with before treatment,Fib (14 d after treatment),PLT,and hs-CRP were decreased,PT and APTT were prolonged,the NIHSS scores were decreased,and Barthel indexes were increased. There were significant differences (all P<0. 05). At day 14 after treatment,there were significant differences in Fib,PT,APTT,hs-CRP,NIHSS scores,and Barthel indexes (Fib:3. 25 ± 0. 38 g/L vs. 3. 55 ± 0. 28 g/L;PT:15. 7 ± 3. 2 s vs. 12. 9 ± 2. 5 s;APTT:42. 7 ± 3. 5 s vs. 38. 7 ± 2. 6 s;PLT:[189 ± 26]× 109/L vs. [201 ± 23]× 109/L;hs-CRP:5. 7 ± 0. 6 mg/L vs. 11. 3 ± 2. 2 mg/L;NIHSS scores:5. 6 ± 2. 4 vs. 9. 2 ± 4. 5;and Barthel indexes:68 ± 15 vs. 47 ± 5)between the two groups (all P <0. 05). Except 1 patient occurred symptomatic intracerebral hemorrhage after thrombolysis,no other serious complications were observed in the thrombolytic group. One patient in the control group had stress gastric ulcer and bleeding,no symptomatic intracerebral hemorrhage occurred. Conclusion Multimode CT guidance can be used as a reliable imaging evidence for patients with WUS expanding intravenous thrombolytic time window. Under the multimode CT guidance, using rt-PA for intravenous thrombolytic therapy has a certain efficacy.
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Objective: To investigate the effect of tanshinone IIA (TSN) on left ventricular hypertrophy (LVH) and cardiomyocyte apoptosis in spontaneous hypertensive rats (SHRs). Methods: A total of 60 SHRs at 8 weeks of age were randomly divided into 3 group: Blank control group, the rats were sacriifced at 8 weeks, TSN group, the rats were treated with TSN at 1 ml/(kg?d) for 18 weeks and Solvent control group, the rats were treated with the solvent at 1 ml/(kg?d) for 18 weeks. n=20 in each group and 15 rats were used for the experiments. The systolic blood pressure (SBP) and left ventricular mass index (LVMI) were examined, cardiomyocyte’s diameter and surface area were measured by HE staining, the apoptosis rate was evaluated by TUNEL method and the apoptosis related protein expression s of Bcl-2, Bax and p53 were determined by Western blot analysis. Results: ①Compared with Solvent control group, TSN group had decreased LVMI (3.23 ± 0.24) mg/g vs (4.58 ± 0.68) mg/g,cardiomyocyte’s diameter (16.13 ± 1.77) μm vs (27.15 ± 3.52) μm and surface area (230.23 ± 69.37) μm2 vs (490.12 ± 118.96) μm2and decreased apoptosis rate (7.45 ± 1.78) % vs (10.61 ± 2.77) %, allP0.05. Conclusion: TSN could inhibit the development of LVH and decrease the cardiomyocyte apoptosis, which might be via up-regulating the protein expressions of Bcl-2 and down-regulating Bax and p53 in SHRs.
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[ABSTRACT]AIM:Tostudytheprotectiveeffectofbrain-derivedneurotrophicfactor(BDNF)onvascularendo-thelial cells with H 2 O2-induced oxidative injury .METHODS: Human umbilical vein endothelial cells ( HUVECs ) were cultured in vitro, and the oxidation injury model of HUVECs was established by treatment with H 2 O2 .The oxidatively in-jured HUVECs were cultured with different concentrations (1, 10 and 100μg/L) of BDNF.At the same time, the control group (no injury), PBS treatment after H2O2 injury group and TrkB inhibitor group (with 100 μg/L BDNF and 1∶1 000 TrkB inhibitor) were also set up.The viability of the HUVECs was detected by MTT assay .The levels of LDH, MDA, SOD and GSH were measured .The releases of NO , ET-1 and ICAM-1 were analyzed by ELISA .The changes of ROS pro-duction and cell apoptosis were evaluated by flow cytometry .The protein levels of TrkB , p-TrkB, cleaved caspase-3, Bcl-2 and Bax were determined by Western blot .RESULTS:Compared with uninjured control group , in H2 O2 oxidative injury plus PBS treatment group , the viability of the cells was decreased significantly , the LDH and MDA levels were increased significantly and the activities of SOD and GSH were decreased significantly .The NO secretion was decreased , and the ET-1 and ICAM-1 concentrations were increased significantly .The ROS content and apoptotic rate were increased significantly . The protein levels of cleaved caspase-3 and Bax were increased but Bcl-2 protein expression was decreased significantly . Compared with PBS treatment group , in H2 O2-injured HUVECs treated with different concentrations of BDNF , the cell via-bility was gradually increased , the LDH and MDA levels were decreased and the activities of SOD and GSH were increased gradually .The secretion of NO was increased but ET-1 and ICAM-1 were decreased gradually .The ROS content and apop-totic rate were decreased significantly .The TrkB and p-TrkB levels were significantly increased significantly , the protein expression of cleaved-caspase 3 and Bax was decreased gradually and the Bcl-2 protein expression increased gradually .The role of BDNF was inhibited by TrkB inhibitor .CONCLUSION:BDNF protects HUVECs from oxidative injury by binding with TrkB to activate the BDNF-TrkB signaling pathways .
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Quality is the key not only to the competence of the hospital,but also to the "two benefits".It is the essence of the development of the hospital.Aiming at improving the management of the hospital's quality,combining with some experience before,the article discusses on the aspects as follows: change ideal and intensify consciousness,reform system and improve institution,stick to the project and put emphasis on the implement.