Mesenchymal stem cell transplantation improves the prognosis of ischemic stroke:a Meta-analysis / 中国组织工程研究

BACKGROUND: Mesenchymal stem cell (MSC) transplantation has been gradually developed to improve the prognosis of cerebral infarction and its sequelae in clinical trials, which has been identified as effective and safe. A small sample size, however, results in the lack of evidence-based medical evidence.OBJECTIVE: To systematically review the efficacy of MSC transplantation on the prognosis of cerebral infarction. METHODS: In order to collect randomized controlled trials (RCTs) of MSC transplantation for the prognosis of cerebral infarction, we searched Cochrane Library, PubMed, Ovid, CBM, CNKI, WanFang, and VIP Data from its inception to November 2016. Articles addressing MSCs transplantation alone or with conventional drug treatment and/or rehabilitation training versus conventional drug treatment alone or with rehabilitation training were included. Two authors independently screened the literature according to the inclusion and exclusion criteria, extracted data, and assessed the risk of bias. Thereafter, qualitative description and Meta-analysis were performed. RESLUTS AND CONCLUSION: Ten RCTs involving 626 cerebral infarction patients were included in the Meta-analysis. The results showed that the MSCs group was superior to the control group with statistical significance in the daily life ability(Barthel index)[MD=20.06, 95%CI(9.95,30.18),P=0.000 1],motor function(Fugl-Meyer scale)[MD=14.60,95% CI(12.96,16.25),P<0.000 01],personal disability (functional independent measure)[MD=15.16,95%CI(9.06,21.26),P<0.000 01]and neurological deficit score(National Institute of Health stroke scale)[MD=-2.59,95% CI(-3.14,-2.05),P<0.000 01].Low fever and mild headache were reported by four included studies,and waist pain was only by one study, but these symptoms went away by themselves or after symptomatic treatment. Subgroup analysis suggested that MSCs from the bone marrow were superior to those from the umbilical cord and cord blood, but showed a greater heterogeneity. It is suggested that the MSC transplantation ameliorate the prognosis in patients with cerebral infarction, significantly improve the activities of daily living, motor function, personal disability and neurological function, with no presence of serious adverse effects. However, high-quality studies with large sample size are required for further investigation on the clinical application of MSC transplantation.

Evodiamine Inhibits Angiotensin II-Induced Rat Cardiomyocyte Hypertrophy / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the effects of evodiamine (Evo), a component of Evodiaminedia rutaecarpa (Juss.) Benth, on cardiomyocyte hypertrophy induced by angiotensin II (Ang II) and further explore the potential mechanisms.</p><p><b>METHODS</b>Cardiomyocytes from neonatal Sprague Dawley rats were isolated and characterized, and then the cadiomyocyte cultures were randomly divided into control, model (Ang II 0.1 μmol/L), and Evo (0.03, 0.3, 3 μmol/L) groups. The cardiomyocyte surface area, protein level, intracellular free calcium ([Ca]) concentration, activity of nitric oxide synthase (NOS) and content of nitric oxide (NO) were measured, respectively. The mRNA expressions of atrial natriuretic factor (ANF), calcineurin (CaN), extracellular signal-regulated kinase-2 (ERK-2), and endothelial nitric oxide synthase (eNOS) of cardiomyocytes were analyzed by real-time reverse transcriptionpolymerase chain reaction. The protein expressions of calcineurin catalytic subunit (CnA) and mitogen-activated protein kinase phosphatase-1 (MKP-1) were detected by Western blot analysis.</p><p><b>RESULTS</b>Compared with the control group, Ang II induced cardiomyocytes hypertrophy, as evidenced by increased cardiomyocyte surface area, protein content, and ANF mRNA expression; increased intracellular free calcium ([Ca]) concentration and expressions of CaN mRNA, CnA protein, and ERK-2 mRNA, but decreased MKP-1 protein expression (P<0.05 or P<0.01). Compared with Ang II, Evo (0.3, 3 μmol/L) significantly attenuated Ang II-induced cardiomyocyte hypertrophy, decreased the [Ca] concentration and expressions of CaN mRNA, CnA protein, and ERK-2 mRNA, but increased MKP-1 protein expression (P<0.05 or P<0.01). Most interestingly, Evo increased the NOS activity and NO production, and upregulated the eNOS mRNA expression (P<0.05).</p><p><b>CONCLUSION</b>Evo signifificantly attenuated Ang II-induced cardiomyocyte hypertrophy, and this effect was partly due to promotion of NO production, reduction of [Ca]i concentration, and inhibition of CaN and ERK-2 signal transduction pathways.</p>

Rutaecarpine inhibits angiotensin II-induced proliferation in rat vascular smooth muscle cells / 中国结合医学杂志

<p><b>OBJECTIVE</b>To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin II (Ang II)-induced proliferation in cultured rat vascular smooth muscle cells (VSMCs).</p><p><b>METHODS</b>VSMCs were isolated from Male Sprague-Dawley rat aorta, and cultured by enzymic dispersion method. Experiments were performed with cells from passages 3-8. The cultured VSMCs were randomly divided into control, model (Ang II 0.1 μmol/L), and rutaecarpine (0.3-3.0 μmol/L) groups. VMSC proliferation was induced by Ang II, and was evaluated by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and cell counting. To examine the mechanisms involved in anti-proliferative effects of rutaecarpine, nitric oxide (NO) levels and NO synthetase (NOS) activity were determined. Expressions of VSMC proliferation-related genes including endothelial nitric oxide synthase (eNOS), and c-myc hypertension related gene-1 (HRG-1) were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>Rutaecarpine (0.3-3.0 μmol/L) inhibited Ang II-induced VSMC proliferation and the best effects were achieved at 3.0 μmol/L. The Ang II-induced decreases in cellular NO contents and NOS activities were antagonized by rutaecarpine (P <0.05). Ang II administration suppressed the expressions of eNOS and HRG-1, while increased c-myc expression (P <0.05). All these effects were attenuated by 3.0 μmol/L rutaecarpine (P <0.05).</p><p><b>CONCLUSION</b>Rutaecarpine is effective against Ang II-induced rat VSMC proliferation, and this effect is due, at least in part, to NO production and the modulation of VMSC proliferation-related gene expressions.</p>

Protective effect of Ginkgo biloba leaf extract on learning and memory deficit induced by aluminum in model rats / 中国结合医学杂志

<p><b>OBJECTIVE</b>To examine the protective effect of Ginkgo biloba leaf extract (GbE) on learning and memory deficit induced by aluminum chloride (AlCl(3)), and explore its mechanisms.</p><p><b>METHODS</b>The rat models with learning and memory deficit were induced by administering via gastrogavage and drinking of AlCl(3) solution. And the model rats were treated with GbE at the dose of 50, 100, 200 mg/kg every day for 2 months accompanied with drinking of AlCl(3) solution, respectively. Their abilities of spatial learning and memory were tested by Morris water maze, and the acetylcholinesterase (AChE) activity in serum was assayed with chemical method, the AChE expression in hippocampus was observed by immunohistochemistry assay, and then quantitative analysis was done by BI 2000 image analysis system.</p><p><b>RESULTS</b>Learning and memory deficit of rats could be induced by AlCl(3) solution (P < 0.01), and AChE expressions in rats hippocampus were increased (P < 0.01); GbE ameliorated learning and memory deficit and reduced AChE expression in rats hippocampus in a dose-dependent manner, while GbE significantly increased serum AChE activity at the dose of 200 mg/kg each day (P < 0.05).</p><p><b>CONCLUSION</b>GbE can ameliorate learning and memory deficit induced by AlCl(3), which may be due to its inhibition of the AChE expression in hippocampus.</p>

Protective effect of ecdysterone on PC12 cells cytotoxicity induced by beta-amyloid25-35 / 中国结合医学杂志

<p><b>OBJECTIVE</b>To examine the protective effect of ecdysterone (ECR) against beta-amyloid peptide fragment(25-35) (Abeta(25-35))-induced PC12 cells cytotoxicity, and to further explore its mechanism.</p><p><b>METHODS</b>Experimental PC12 cells were divided into the Abeta group (treated by Abeta(25-35) 100 micromol/L), the blank group (untreated), the positive control group (treated by Vit E 100 micromol/L after induction) and the ECR treated groups (treated by ECR with different concentrations of 1, 50 and 100 micromol/L). The damaged and survival condition of PC12 cells in various groups was monitored by lactate dehydrogenase (LDH) release and MTT assay. The content of malondialdehyde (MDA) was measured by fluorometric assay to indicate the lipid peroxidation. And the antioxidant enzymes activities in PC12 cells, including superoxide dismutases (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), were detected respectively.</p><p><b>RESULTS</b>After PC12 cells were treated with Abeta(25-35) (100 micromol/L) for 24 hrs, they revealed a great decrease in MTT absorbance and activity of antioxidant enzymes, including SOD, CAT and GSH-Px as well as a significant increase of LDH activity and MDA content in PC12 cells (P < 0.01). When the cells was pretreated with 1-100 micromol/L ECR for 24 hrs before Abeta(25-35) treatment, the above-mentioned cytotoxic effect of Abeta(25-35) could be significantly attenuated dose-dependently, for ECR 50 micromol/L, P < 0.05 and for ECR 100 micromol/L, P < 0.01. Moreover, ECR also showed significant inhibition on the Abeta(25-35) induced decrease of SOD and GSH-Px activity, but not on that of CAT.</p><p><b>CONCLUSION</b>ECR could protect PC12 cells from cytotoxicity of Abeta(25-35), and the protective mechanism might be related to the increase of SOD and GSH-Px activities and the decrease of MDA resulting from the ECR-pretreatment.</p>