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China Pharmacy ; (12): 3065-3068, 2017.
Artigo em Chinês | WPRIM | ID: wpr-618244

RESUMO

OBJECTIVE:To study the improvement effect of Poria cocos peels water extract(PWE)on liver fibrosis in rats in-duced by carbon tetrachloride(CCl4). METHODS:84 rats were randomly divided into blank control group,solvent control group, model control group, positive control group (Compound biejia ruangan tablet, 0.75 g/kg), PWE low-dose, medium-dose, high-dose groups (0.9,1.8,3.6 g/kg,calculated by crude drugs),12 in each group. Except for blank control group and solvent control group(ip vegetable oil),other groups received CCl4-vegetable oil solution to reduce liver fibrosis model,ip. After model-ing,each administration group received related medicines,ig,other 3 groups received equal volume of normal saline,once a day, for 4 weeks. After administration,enzyme-linked immunosorbent assay was used to detect the aspartate aminotransferase(AST),al-anine aminotransferase(ALT),laminin(LN),hyaluronic acid(HA),hydroxyproline(Hyp)contents in serum and reduced gluta-thione (GSH),superoxide dismutase (SOD),malondialdehyde (MDA) contents in liver tissue of rats;HE staining and Masson staining were adopted to observe the pathological changes of liver tissue. RESULTS:Compared with blank control group,indexes of rats in solvent control group had no obvious changes(P>0.05). AST,ALT,LN,HA,Hyp contents in serum and MDA con-tent in liver tissue in model control group were significantly increased(P<0.05);GSH,SOD contents in liver tissue were signifi-cantly reduced(P<0.05);and liver tissue showed obvious fibrosis lesions. Compared with model control group,AST,ALT,LN, HA,Hyp contents in serum and MDA content in liver tissue in PWE medium-dose,high-dose groups were significantly reduced (P<0.05);GSH,SOD contents in liver tissue were significantly increased(P<0.05);fibrosis degree of liver tissue was obvious-ly relieved. CONCLUSIONS:PWE shows good improvement effect on liver fibrosis of rats induced by CCl4,which may be related to inhibiting the lipid peroxidation.

2.
China Pharmacy ; (12): 3505-3508, 2016.
Artigo em Chinês | WPRIM | ID: wpr-504962

RESUMO

OBJECTIVE:To investigate the effects of Astragalus polysaccharides on heart function and myocardial fibrosis in spontaneously hypertensive rats (SHR) and corresponding mechanism. METHODS:50 SHR were randomly divided into a model group,a captopril tablets group (positive drug,30 mg/kg) and the groups of high,medium and low-dose (100,50,25 mg/kg) Astragalus polysaccharides,with 10 SHR in each group. Another 10 Wistar Kyoto rats were included into the normal group. The rats in the drug administration groups were given corresponding drugs ip,while those in the normal group and the model group were given isometric distilled water ip,once a day,for 12 consecutive weeks. The left ventricular systolic pressure (LVSP),left ventricular end diastolic pressure (LVEDP),left ventricular pressure rise rate (+dp/dtmax) and left ventricular pressure decline rate (-dp/dtmax) of the rats were recorded. The heart mass index (HMI) and left ventricular mass index (LVMI) thereof were deter-mined. The level of hydroxyproline and the mRNA and protein expression of transforming growth factor-β1(TGF-β1)and peroxi-some proliferator-activated receptor-γ(PPAR-γ)in the cardiac muscle tissue thereof were detected. RESULTS:Compared to the nor-mal group,the rats in the model group had lower LVSP,+dp/dtmax and-dp/dtmax,higher LVEDP,HMI and LVMI,as well as high-er levels of hydroxyproline and the mRNA and protein expression of TGF-β1 and lower level of the mRNA and protein expression of PPAR-γ in the cardiac muscle tissue (P0.05) in all the above-mentioned indexes was shown between the model group and the group of low-dose Astragalus polysaccha-rides,except that the-dp/dtmax of the latter was significantly higher and the level of the mRNA expression of TGF-β1 was obvious-ly lower (P<0.05). CONCLUSIONS:Astragalus polysaccharide can improve heart function and myocardial fibrosis in SHR by a mechanism which may be related to downregulating the expression of TGF-β1 and upregulating the expression of PPAR-γin the car-diac muscle tissue.

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