Objective To explore the clinical efficacy of ganglion glycosides combined with edaravone in the treatment of patients with acute cerebral infarction(ACI),to assess the improvement of neurological function and prognosis.Methods 240 ACI patients were selected.They were randomly divided into control group (120 cases) and observation group(120 cases) by random number table.The control group received edaravone treatment,the observation group received ganglion glycosides combined with edaravone treatment.Assessed the clinical efficacy,neurological and physical features by National Institutes of Health Stroke Scale (NIHSS),Glasgow Coma Scale score (GCS) and (Fug -Meyer,FM) score.Results The NIHSS score of the observation group after treatment was (23.71 ± 6.08) points,which was lower than (26.50 ± 6.12) points of the control group.The FM and GCS scores of the observation group were (15.20 ± 1.81) points and (77.89 ± 10.15) points respectively,which were higher than (13.29 ± 1.77) points and (13.29 ± 1.77) points of the control group the control group,the differences were statistically significant (t =9.14,8.25,10.37,all P ＜0.05).The total effective rates of the observation group and the control group were 75.00％ (90/120) and 65.00％ (78/120) respectively,the difference was statistically significant between the two groups (x2 =9.64,P ＜ 0.05).Conclusion For ACI patients,treated with ganglion glycosides on the basis of edaravone,the patients' neurologic and limb motor function is improved significantly,the clinical efficacy and prognosis is improved significantly.

AIM: To investigate the relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia reoxygenation and GABA A receptor in primary cultured rat cortical neurons. METHODS: The primary cultured rat cortical neurons were used to make the hypoxia reoxygenation damage model. The morphology of cell was observed. The lactate dehydrogenase (LDH) effluxed into the media as an indicator of neuronal injury was detected after 6 h of the reoxygenation injuries. The malonyldialdehyde (MDA) contents, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were determined at the same time. RESULTS: The hypoxia reoxygenation caused neuronal swelling and widespread neuronal degeneration, increased LDH efflux and MDA contents, and decreased SOD and GPX activities. Sodium oxybate assuaged neuron damage, decreased LDH efflux and MDA contents (P

Objective To investigate the calcium dobesilate tablets combined with mecobalamin injection in treatment of diabetic peripheral neuropathy and effects on oxidative stress and neurotrophic factor.Methods 82 cases of diabetic peripheral neuropathy(DPN) patients from February 2015 to October 2016 in our hospital were selected and randomly divided into observation group and control group with 41 cases in each group.The control group was treated with mecobalamin injection, the observation group were treated with calcium dobesilate tablets.The course of treatment was two weeks in two groups.Results The total efficiency of the observation group (90.24%) was higher than the control group (68.29%) , the difference was statistically significant ( P<0.05 ) , patients in the observation group after the treatment of common peroneal nerve and median nerve SCV and MCV higher than the control group, the difference was statistically significant (P <0.05), the level of serum malondialdehyde (MDA) in the observation group was lower than that in the control group and the level of superoxide dismutase ( SOD) in the observation group was higher than that in the control group, the difference was statistically significant (P<0.05), the levels of serum NGF and BDNF in the observation group were higher than those in the control group, the difference was statistically significant (P<0.05), the two groups were no obvious adverse reactions.Conclusion Calcium dobesilate tablets and mecobalamin injection curative effect in the treatment of diabetic peripheral neuropathy , and patients could improve oxidative stress and neurotrophic factors, and the safety is good, has the important research significance.

Objective:To correlate homocysteine (Hcy) and blood lipid levels with neurological function in patients with progressive ischemic stroke.Methods:A total of 400 patients with ischemic stroke who received treatment between June 2018 and June 2020 in Linhai Second People's Hospital were included in this study. Progressive ischemic stroke ( n = 126) and non-progressive ischemic stroke ( n = 274) groups were designated. Hcy level was determined by enzyme-linked immunosorbent assay. High-density lipoprotein cholesterol, triacylglycerol, low-density lipoprotein cholesterol and cholesterol levels were measured using a biochemical analyzer. Hcy and blood lipid levels as well as National Institute Health of Stroke Scale (NIHSS) score were determined in each group. Hcy and blood lipid levels were correlated with NIHSS score. Results:Hcy level in the progressive ischemic stroke group was significantly higher than that in the non-progressive ischemic stroke group [(28.39 ± 4.36) μmol/L vs. (20.17 ± 3.24) μmol/L, t = 18.894, P < 0.05]. Low-density lipoprotein cholesterol , triacylglycerol and TC levels in the progressive ischemic stroke group were (3.29 ± 0.45) mmol/L, (2.08 ± 0.34) mmol/L and (4.82 ± 0.79) mmol/L, respectively, which were significantly higher than those in the non-progressive ischemic stroke group [(2.48 ± 0.37) mmol/L, (1.56 ± 0.29) mmol/L and (4.08 ± 0.43) mmol/L, t = 17.644, 14.859, 9.860, P < 0.05]. High-density lipoprotein cholesterol level in the progressive ischemic stroke group was significantly lower than that in the non-progressive ischemic stroke group [(1.03 ± 0.13) mmol/L vs. (1.19 ± 0.14) mmol/L, t =11.158, P < 0.05]. NIHSS score in the progressive ischemic stroke group was significantly higher than that in the non-progressive ischemic stroke group [(21.72 ± 4.35) points vs. (15.52 ± 2.89) points, t = 14.582, P < 0.05]. Hcy, low-density lipoprotein cholesterol, cholesterol and triacylglycerol levels were linearly and positively correlated with NIHSS score ( r = 0.846, 0.724, 0.718, 0.765, all P < 0.05), while igh-density lipoprotein cholesterol level was linearly and negatively correlated with NIHSS score ( r = -0.710, P < 0.05). Conclusion:In patients with progressive ischemic stroke, Hcy level is increased and blood lipid level is obviously abnormal. Hcy and blood lipid levels are greatly correlated with neurological function.

OBJECTIVE: To explore the effects of matrine on the proliferation, tumor cell stemness, β-catenin transcriptional activity and AKT/GSK3β/β-catenin signaling pathway in human hepatocellular carcinoma (HCC) HepG2 and Huh7 cells. METHODS: The proliferation and colony formation ability of HepG2 and Huh7 cells treated with 200, 400, and 800 μg/mL matrine were evaluated with MTT assay and colony formation assay, respectively. Real-time quantitative PCR was performed to detect the mRNA expressions of CD90, epithelial cell adhesion molecule (EpCAM) and CD133, and dual-luciferase assay was used to detect the transcriptional activity of β-catenin in the treated cells. The effects of matrine on the expressions of protein kinase B (AKT), P-AKT, GSK-3β, P-GSK-3β, P-β-catenin and β-catenin proteins in the Wnt/β-catenin signaling pathway were assessed using Western blotting. RESULTS: Matrine inhibited the proliferation of the two HCC cell lines in a time- and concentration-dependent manner. The half-inhibitory concentrations of matrine were 2369, 1565 and 909.1 μg/mL at 24, 48 and 72 h in HepG2 cells, respectively, and were 1355, 781.8, and 612.8 μg/mL in Huh7 cells, respectively. Matrine concentrationdependently suppressed colony formation of the HCC cells, producing significant inhibitory effects at 400 μg/mL < 0.01) and 800 μg/mL < 0.001) in HepG2 cells and at 200 μg/mL < 0.05), 400 μg/mL < 0.01), and 800 μg/mL < 0.001) in Huh7 cells. Matrine at 400 and 800 μg/mL significantly inhibited the mRNA expression of CD90, EpCAM and CD133 and the transcriptional level of β-catenin in both HepG2 and Huh7 cells < 0.05 or 0.01). Matrine at 400 and 800 μg/mL also significantly decreased the protein levels of β-catenin, P-AKT and P-GSK-3β and increased the phosphorylation level of β-catenin in both of the cell lines. CONCLUSIONS Matrine inhibits the proliferation, colony formation, and the expressions of tumor stem cell markers CD90, EpCAM and CD133 in both HepG2 and Huh7 cells probably by inhibiting Wnt/β-catenin signaling pathway and the transcriptional activity ofβ-catenin.