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1.
Chinese Pharmacological Bulletin ; (12): 261-265,266, 2015.
Article in Chinese | WPRIM | ID: wpr-600732

ABSTRACT

Aim To investigate the protective effects of total triterpenoid from Prunella vulgaris L. ( TTP) on CCl4-induced hepatic fibrosis in rats and its mecha-nism. Methods Rat liver fibrosis was induced by 50% CCl4 twice a week for 12 weeks. From the 5th week, all the therapeutic groups were treated with the TTP(25, 50, 100 mg·kg-1 ) and the colchicine (0. 1 mg· kg-1 ) respectively once a day for 8 weeks. At the end of the twelfth week, the levels of ALT, AST, HA, PCⅢ, CⅣ, MDA, SOD, GSH-Px, Hyp were measured . HE and Masson staining were used to evalu-late the degree of hepatic fibrosis. The mRNA expres-sion ofα-SMA, procollagen I, Smad2, Smad3, Smad7 in liver was detected by RT-PCR, and the p-ERK pro-tein expression was evaluated by Western blot. Results Compared with the model group, TTP(25, 50, 100 mg·kg-1 ) not only reduced serum content of ALT, AST, HA, PCⅢ, CⅣand Hyp, MDA in liver tissue, improved the morphologic changes of hepatic fibrosis, but also increased SOD and GSH-Px activity. Moreo-ver, it decreased the α-SMA, procollagen I, Smad2, Smad3 mRNA expression and increased Smad7 mRNA expression in liver tissues obviously. Furthermore, TTP reduced the protein expression of p-ERK. Conclusions TTP can protect rats from CCl4-induced liver fibro-sis. The mechanism of this process may involve inhibi-ting the expression of p-ERK and interference with TGF-β1/Smad signal transduction pathway.

2.
Journal of Kunming Medical University ; (12): 63-66, 2013.
Article in Chinese | WPRIM | ID: wpr-438435

ABSTRACT

Objective To observe the effect of combination therapies with methotrexate, sulfasalazine and hydroxychloroquine on hyperlipemia of rheumatoid arthritis.Method From 2009 November to 2010 November, 68 RA inpatients and outpatients in the department of rheumatism of our hospital were randomly divided into two groups: A group and B group, 34 cases in each group. The patients in A group were given combination of methotrexate, sulfasalazine, hydroxychloroquine sulfate for the treatment of RA,patients in B group, based on A group's treatment, were treated by xuezhikang. Some indexes were observed in two group before treatment and 6 months after treatment, including cholesterolTC,low density lipoprotein cholesterol LDL-C , triglyceride TG , high density lipoprotein cholesterol HDL-C , swelling index, joint pain index, time of morning stiffness, C-reactive protein CRP , erythrocyte sedimentation rate ESR and DAS28. Results After 6 months’ treatment, the serum levels of TC, TG,, LDL-C, both in two groups of patients, were lower than those before treatment, and HDL-C was higher than that before treatment, there were significant differences (P0.05) . Conclusion RA patients have abnormal blood lipid levels, disease-modifying anti-rheumatic drugs have effect on blood lipid during remission joint disease in RA patients.

3.
Chinese Journal of Geriatrics ; (12): 423-425, 2013.
Article in Chinese | WPRIM | ID: wpr-436236

ABSTRACT

Objective To explore the effects of psychological intervention on negative emotions and quality of life in patients with rheumatoid arthritis (RA).Methods A total of 112 patients with rheumatoid arthritis were divided into two groups:the intervention group and the control group.All patients were given drugs for treatment of RA.Additionally,patients in the intervcntion group were received psychological intervention.Zung's self-rating depression scale (SDS),Zung's self-rating anxiety scale (SAS),RA disease activity score (DAS28),visual analog scale (VAS),disability index of health assessment questionnaire (HAQ-DI) were assessed,and the related laboratory parameters such as erythrocyte sedimentation rate (ESR),C reactive protein (CRP),rheumatoid factor (RF)were determined.Results 6 months after the treatment,there were significant differences in SDS and SAS between the treatment group and the control group [SDS:(31.7±4.7)scores vs.(29.6±4.4)scores; SAS:(34.7±5.3)scoresvs.(32.6±5.1)scores; t=2.441,-2.119,both P<0.05].The patients with tender joints,joint swelling and morning stiffness time were less in the treatment group than in control group [(5±3) vs.(7±4),(4±3) vs.(5±3),(36±16) min vs.(42±19)min.respectively,t=2.054,2.393,1.995,all P<0.05].The scores of HAQ-DI,VAS and DAS28were lower in the treatment group than in control group [(0.89±0.73) vs.(1.20±0.77),(6.1±1.6) vs.(6.8±1.8),(3.2±1.7) vs.(3.9±1.9),respectively,t=2.136,2.406,2.135,all P<0.05].There was a significant difference in CRP between the treatment group and the control group [(34±14) mg/L vs.(37± 17)mg/L,t=2.406,P<0.05].Conclusions Psychological intervention can improve the negative emotions and quality of life in patients with rheumatoid arthritis.

4.
Chinese Pharmacological Bulletin ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-565851

ABSTRACT

Aim To explore the anti-fibrotic effect of Oxymatrine(OM) on CCl4-induced liver fibrosis in rats and its modulation on the TGF-?1.Methods A hepatic fibrosis model was induced by CCl4.The levels of Alanine transaminase(ALT),aspartic transaminase(AST),type-Ⅰ collagen and TGF-?1 in plasma were detected by chemical Kit.The deposition of collagen was observed with H&E and Masson staining.Pathological changes were observed under light microscope in 8 randomly selected fields in each group.RT-PCR method was applied to detect the expression of TGF-?1 mRNA in hepatic tissue.Results The concentration of serum ALT,AST,type-Ⅰ collagen and TGF-?1 was significantly reduced in the middle and high dose treated groups compared with that of model group.A significant reduction of collagen deposition and rearrangement in OM-treated group was displayed in histopathological changes.The expression of TGF-?1 mRNA was considerably decreased in the treated animals.Conclusions Oxymatrine is effective in reducing the production and deposition of collagen in the liver tissue of experimental groups,and it has an obvious protective effect on model rats.It may be one of the therapeutic mechanisms to modulate the expression of TGF-?1 mRNA.

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