Objective To study the effect of lienal polypeptide injection on immune function in patients with chronic kidney disease(stage CKD5,uremia).Methods 42 patients with maintenance hemodialysis and 42 patients with peritoneal dialysis in stage CKD5 phase were selected as the research subjects.According to the digital table,they were randomly divided into observation group and control group,32 cases in each group.All patients were treated with hemodialysis or peritoneal dialysis,the observation group was treated with lienal polypeptide injection,while the con-trol group was treated without lienal polypeptide injection.The immune function index(CD3+,CD4+,CD8+,CD4+/CD8+) were compared between the two groups after treatment for 15 d.Results In the observation group,the immune index after 15 days treatment were CD3+(58.26 ±7.90)%,CD4+(34.46 ±6.45)%,CD8+(25.33 ±4.47)%,CD4+/CD8+(81.36 ±0.21).In the control group,the immune index after 15 days treatment were CD3+(55.64 ±5.32)%,CD4+(31.79 ±7.15)%,CD8+(27.52 ±4.68)%,CD4+/CD8+(1.16 ±0.18).CD3+,CD4+,CD4+/CD8+ levels of the obser-vation group were significantly higher than those of the control group(t =2.820,t =1.610,t =7.060,all P <0.05). The level of CD8+ was significantly lower than that of the control group(t =0.004,P <0.05).Conclusion Lienal polypeptide can effectively improve the immune function of patients with chronic kidney disease (CKD5 stage).

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.

[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 .

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) %, allP<0.01.②With NAPDH reference correction, compared with Solvent control group, TSN group presented increased protein expression of Bcl-2 (0.97 ± 0.31) vs (0.40 ± 0.11) and decreased Bax (0.37 ± 0.15) vs (1.81 ± 0.44), decreased p53 (0.83 ± 0.18) vs (2.72 ± 0.28), allP<0.05 or P<0.01. The above indexes were similar between TSN group and Blank control group,P>0.05. 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.

Objective To investigate the effect of erythropoietin(EPO)on the proliferation of neural stem cells(NSCs)derived from central canal of adult rat spinal cord in vitro ,so as to provide a theoretical basis for clinical treatment of spinal cord injury by autotransplanting or allograft transplanting of adult spinal cord NSCs. Method NSCs were isolated from the central canal of the adult rats spinal cord by microsurgical method,and Nestin(nestin)and Sox2 immunofluorescence stain were used to identify the cells. After cells were treated with different dose of EPO,5,10,20 and 40 U/mL,respectively,the optical treatment concentration and time were determined by CCK8 assay. The effect of EPO on the cell count and the expression of Cyclin D1 in NSCs were detected at the treatment time 96 h. Result The NSCs derived from the central canal of adult SD rats spinal cord could stably express protein Nestin and transcription factor Sox2. As the results of CCK8 test,cell counts and real-time quantitative PCR showed the optimal treatment of concentration and time maybe 20 U/mL and 96 h. Conclusions This study shows that EPO can promote the proliferation of NSCs derived from central canal of adult rat spinal cord,and the optimal treatment of concentration and time for proliferation might be 20 U/mL and 96 h.