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Chinese Journal of Experimental Traditional Medical Formulae ; (24): 131-136, 2020.
Article in Chinese | WPRIM | ID: wpr-873064

ABSTRACT

Objective:To observe the effects of adjuvant therapy of Huayu pills on neurological recovery of patients with acute cerebral infarction (ACI) and syndrome of Qi deficiency and blood stasis, and to investigate its mechanism of action for antioxidation, anti-inflammation and improvement of microcirculation. Method:One hundred and forty patients were randomly divided into control group (70 cases) and observation group (70 cases) by random number table. During the study period, there were 3 drop-out cases, 2 excluded cases, and 65 completed cases in the control group. There were 1 drop-out cases, 4 excluded case, and 65 completed cases in the observation group. Western medicine was given in both groups. Patients in control group additionally got oral administration of Xiaoshuang Tongluo tablets, 6 tablets/time, 3 times/day. The patients in observation group got oral administration of Huayu pills, 5 g/time, 2 times/days. The treatment course was 4 weeks in both groups. Before the treatment, and at the second and fourth week after treatment, scores of national institute of health stroke scale (NIHSS) were graded. Before and after treatment, scores of functional independent measures (FIM) scale, fugl-meyer assessment of motor function (FMA), Qi deficiency and blood stasis syndrome were graded. Disability/mortality and safety were discussed after treatment. Levels of the whole blood viscosity (BV), plasma viscosity (PV), platelet aggregation rate (PAG), fibrinogen (FIB), P-selectin (CD62p), D-dimer (D-D), superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), lipid peroxide (PLO), homocysteine (Hcy), tumor necrosis factor -α (TNF-α), serum cystatin C (Cys-C) and hypersensitive C-reactive protein (hs-CRP) were detected both before and after treatment. Result:In the analysis of rank sum test, clinical efficacy in observation group was better than that in control group (Z=2.131, P<0.05). At the second and fourth week after treatment, scores of NIHSS, Qi deficiency and blood stasis, as well as levels of NO, PLO, MDA, Hcy, Cys-C, hs-CRP, TNF-α, BV, PV, PAG, FIB, CD62 p and D-D in observation group were lower than those in control group (P<0.01), while levels of FIM, FMA and SOD were all higher than those in control group (P<0.01). Conclusion:Based on the comprehensive treatment of Western medicine, adjuvant therapy of Huayu pills can improve the degree of nerve function defect, improve the ability of exercise and daily life, reduce the degree of disability, improve the microcirculation and hemorheology, reduce the inflammatory reaction, eliminate oxygen free radicals, and relieve the oxidative stress injury in patients with ACI and Qi deficiency and blood stasis syndrome, and the clinical efficacy is better than that of Western medicine alone.

2.
Biomedical and Environmental Sciences ; (12): 786-793, 2014.
Article in English | WPRIM | ID: wpr-270539

ABSTRACT

<p><b>OBJECTIVE</b>To assess the effect of atorvastatin on lipopolysaccharide (LPS)-induced TNF-α production in RAW264.7 macrophages.</p><p><b>METHODS</b>RAW264.7 macrophages were treated in different LPS concentrations or at different time points with or without atorvastatin. TNF-α level in supernatant was measured. Expressions of TNF-α mRNA and protein and heme oxygenase-1 (HO-1) were detected by ELISA, PCR, and Western blot, respectively. HO activity was assayed.</p><p><b>RESULTS</b>LPS significantly increased the TNF-α expression and secretion in a dose- and time-dependent manner. The HO-1 activity and HO-1 expression level were significantly higher after atorvastatin treatment than before atorvastatin treatment and attenuated by SB203580 and PD98059 but not by SP600125, suggesting that the ERK and p38 mitogen-activated protein kinase (MAPK) pathways participate in regulating the above-mentioned effects of atorvastatin. Moreover, the HO-1 activity suppressed by SnPP or the HO-1 expression inhibited by siRNA significantly attenuated the effect of atorvastatin on TNF-α expression and production in LPS-stimulated macrophages.</p><p><b>CONCLUSION</b>Atorvastatin can attenuate LPS-induced TNF-α expression and production by activating HO-1 via the ERK and p38 MAPK pathways, suggesting that atorvastatin can be used in treatment of inflammatory diseases such as sepsis, especially in those with atherosclerotic diseases.</p>


Subject(s)
Animals , Mice , Adjuvants, Immunologic , Pharmacology , Atorvastatin , Enzyme Activation , Heme Oxygenase-1 , Genetics , Metabolism , Heptanoic Acids , Pharmacology , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Pharmacology , Lipopolysaccharides , Pharmacology , Macrophages , Membrane Proteins , Genetics , Metabolism , Pyrroles , Pharmacology , Tumor Necrosis Factor-alpha , Metabolism
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