Abstract:Aim To investigate the effect of Ginsenoside Rg1 on the improvement of nerve function in rats with Cerebral ischemia reperfusion and its mechanism. Methods Wistar rats with ischemia reperfusion injury were randomly divided into sham group, model group, edaravone group (3.2 mg/kg), low (10 mg), medium (20 mg) and high (50 mg) dose groups. At 1 d, 7 d and 14 d after administration, modified m-nss method was used to score neurological defects, and triphenyltetrazolium chloride (TTC) staining was used to determine the volume of cerebral infarction. TUNEL assay In situ was used to detect neuronal apoptosis in brain tissue. Immunohistochemistry was used to detect the levels of NF- kB and GAFP. The expression levels of FZD1, PIWIL1, FOXM1 mRNA and protein were detected by RT-PCR and Western Blot. Results Compared with model control group, the m-NSS were significantly decreased in low dose ginsenoside Rg1 group (P<0.05); the m-NSS were significantly decreased in medium and high dose groups (P<0.01); in low,medium and high dose ginsenoside Rg1 groups, the nerve apoptosis cells were significantly decreased (P<0.01), brain infarct volume were significantly reduced (P<0.01), the expression of NF-κB and GAFP were significantly decreased(P<0.01); The mRNA and protein expressions of FZD1, FOXM1 were significantly increased (P<0.01); The mRNA and protein expressions of PIWIL1 were significantly decreased (P<0.01). Conclusions Ginsenoside Rg1 can significantly improve the neural function of rats with Cerebral ischemia reperfusion. It may be achieved by regulating the expression of FZD1, PIWIL1, FOXM1 genes and proteins.

Abstract:Aim The purpose of this study was to explore the influence of serum non-high-density lipoprotein cholesterol (non-HDLC) on neurologic impairment in patients with acute ischemic stroke and its clinical value in disease risk assessment. Methods A total of 611 cases of acute ischemic stroke patients were recruited in this study. NIHSS(National Institute of Health stroke scale), CSS(China Stroke scale), ESS(Europe Stroke Scale) and BI(Barthel Index) were used to evaluate the degree of neurologic impairments. Fasting plasma glucose(FPG), hypersensitive c-reactive protein(hs-CRP), glycosylated hemoglobin (HbA1c), homocysteine (Hcy), total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDLC) and low density lipoprotein cholesterol (LDLC) were measured in all the patients. Then the density of non-HDLC were calculated with the formula of TC minus HDLC. Results Patients with high level of serum non-HDLC had bigger body mass index, higher NIHSS, CSS and BI scores, lower ESS and elevated TC, TG, LDLC, Hcy, FPG, HbA1c, lower HDLC levels. The NIHSS scores changed corresponding with serum non-HDLC level in acute ischemic stroke patients, the total scores of NIHSS, CSS were positively correlated with the serum non-HDLC level, and the total scores of ESS, and BI were negatively correlated with it. High serum level of non-HDLC was an independent risk factor for neurologic impairment in patients with acute ischemic stroke, when serum non-HDLC elevated to borderline high level, the risk of neurologic impairment significantly increased. Conclusion Increased serum non-HDLC level was an independent risk factor of neurologic impairment in patients with acute cerebral ischemia, it would be an effective indicator, and target of the prevention and treatment as well, of risk prediction for neurologic impairment in patients with acute cerebral ischemia.

Abstract:Aim To observe the change of plasma nitric oxide (NO) of acute cerebral infracted patients and the influence of simvastatin on the level of plasma NO. Methods Using HNO3 deoxidize enzyme method, we examined the levels of plasma NO in 54 patients with cerebral infarction (They were devided into two groups at random: 31 patients in simvastatin therapy group and 23 patients in ordinary therapy group) and 37 normal controls. At the same time, we scored the neurologic impairment of the patients before and after the therapy. Results In cerebral infarction group, the level of plasma NO was significantly higher than the controls at 3d (P< 0.05). After 3 weeks of therapy, the level of plasma NO was not notably different between ordinary therapy group and controls (P> 0.05). While, in simvastatin therapy group, the level of plasma NO was higher than the ordinary therapy group ( P< 0.05). It was significantly different between the two therapy groups about neurologic impairment score after therapy ( P< 0.01). Conclusion The level of plasma NO in patients with acute cerebral infarction might be a reference index for cerebral ischemic damage. Simvastatin can raise the level of plasma NO and improve cerebral infarction prognosis.