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1.
China Pharmacist ; (12): 429-433, 2017.
Article in Chinese | WPRIM | ID: wpr-510100

ABSTRACT

Objective:To study the protective effects of Danhong injection ( DH) on myocardial damage induced by doxorubicin ( DOX) in Lewis tumor bearing mice. Methods:The model of Lewis lung cancer in mice was established by underarm injecting tumor cells, and then randomly divided into four groups:the model control group, DOX group, DH group and DH+DOX group. After the experiment, myocardial and tumor tissue were separated from Lewis tumor bearing mice, and the excised tumors were weighted. The activities of lactate dehydrogenase ( LDH) , creatine kinase ( CK) , manganese superoxide dismutase ( SOD) , catalase ( CAT) and glu-tathione peroxidase ( GPx) , and the content of malondialdehyde ( MDA) were determined by a colorimetric method. Flow cytometry was used to determine the levels of apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential (△Ψm). Re-sults:Compared with that in the model control group, a significant decrease of tumor weight was shown in both DOX group and DH+DOX group (P<0. 01). DH had no significant influence on the anticancer function of DOX. The activity of LDH and CK, and the ap-optosis in myocardium cells significantly increased (P<0. 01). Compared with DOX group, the activities of LDH and CK, and the ap-optosis significantly decreased in DH+DOX group (P<0. 01). The activities of △Ψm, SOD, CAT and GPx significantly increased (P<0.05orP<0.01). ThecontentofMDAandROSgenerationbothdecreased(P<0.01).Conclusion:DHhasnosignificantin-fluence on the antitumor effect of DOX. The combination of DH and DOX shows cadioprotective effect on the myocardial damage through improving mitochondrial antioxidant defense capacity, ameliorating oxidative stress and maintaining △Ψm homeostasis.

2.
International Journal of Traditional Chinese Medicine ; (6): 908-913, 2016.
Article in Chinese | WPRIM | ID: wpr-504060

ABSTRACT

Objective To compare the therapeutical effect of puerarin, ligustrazine, ginsenoside Rb1, Hydroxysafflor yellow A on cerebral ischemia reperfusion mice. Methods The mice were randomly assigned for sham group, model group, puerarin group, ligustrazine group, ginsenoside Rb1 group, and Hydroxysafflor yellow A group, 24 mice for each group. All the groups were subjected to middle cerebral artery occlusion (MCAO) by 1 h ischemia and 24 h of reperfusion except the sham group. The puerarin, ligustrazine, ginsenoside Rb1, Hydroxysafflor yellow A were administrated by tail vein injection with 3μmol/kg at the onset of 1 h of ischemia. The neurologic deficit score, infarct area calculated by TTC staining, cerebral cortex blood flow monitored by laser doppler flowmetry, NO content measured by chemical colorimetry and western blot were applied to determine the expression for cleaved-caspase-3 and nuclear transcription factor NF-κB for each group. Results Compared with the model group, the infarct area (15.83%± 1.83%, 22.00%± 2.53%, 22.83%± 1.83%, 17.83%± 1.72%vs. 34.67%± 2.66%) in the puerarin group, ligustrazine group, ginsenoside Rb1 group, Hydroxysafflor yellow A group was significantly decreased (P<0.01 or P<0.05);the cerebral cortex blood flow (598.81 ± 9.90 μl/kg?min-1, 614.78 ± 9.20 μl/kg?min-1, 577.83 ± 5.55 μl/kg?min-1, 583.54 ± 7.98 μl/kg?min-1 vs. 548.43 ± 1.97 μl/kg?min-1) significantly increased (P<0.01 or P<0.05);the NO content (17.09 ± 1.18μmol/L, 18.54 ± 0.54μmol/L, 18.17 ± 0.49μmol/L, 15.10 ± 0.73μmol/L vs. 20.63 ± 0.73μmol/L) ignificantly decreased (P<0.01 or P<0.05);the expression of cleaved-caspase-3 (1.02 ± 0.08, 1.12 ± 0.04, 0.87 ± 0.08, 1.07 ± 0.08 vs. 1.30 ± 0.06) and NF-κB p-p65/NF-κB p65 (1.03 ± 0.19, 1.15 ± 0.05, 1.12 ± 0.08, 0.72 ± 0.08 vs. 1.45 ± 0.08) ignificantly decreased (P<0.01 or P<0.05) Conclusions Four Chinese herbal monomers could improve nerve and cerebral dysfunctions and ameliorate ischemia symptoms with varying degrees. The mechanisms were involved with the enhancement of cerebral cortex blood flow and inhibition of cell apoptosis and the activation of inflammatory signaling pathways.

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