ABSTRACT
Aim To investigate the protective effects of dihydroquercetin(DDQ) against myocardial ischemis reperfusion injury(MIRI) in rats.Methods Male Sprague-Dawley rats were randomly divided into 4 groups(n=10):normal,control,I/R model, and I/R model+DDQ(5,10 mg·L-1).This study used an isolated Langendorff rat heart model.The left ventricu-lar developed pressure(LVDP),heart rate(HR) and the maximum rise and fall rate of the left ventricular pressure(±dp/dtmax) were monitored and documented using a physiological recorder.The levels of lactate dehydrogenase(LDH) and creatine kinase(CK) were analyzed using enzyme-linked immunosorbent assay(ELISA).Infarct size was measured using 2,3,5-triphenyltetrazolium chloride staining.The levels of superoxide dismutase(SOD) and malondialdehyde(MDA), as well as the ratio of glutathione/glutathione disulfide(GSH/GSSG) were measured via ELISA.HE staining was used to observe the pathological changes of myocardial tissue.Results Compared with the I/R model group, the I/R model+DDQ groups raised hemodynamic parameters, SOD level, and GSH/GSSG ratio;and reduced the amount of CK, LDH, MDA levels.Moreover, the I/R model+DDQ groups had lower infarct size and pathological changes in myocardial tissue than I/R model group.Conclusion DDQ exertes cardioprotective effects against I/R via improving the oxygen free radical scavenging ability, the inhibition of oxygen free radical and reducing lipid peroxidation.
ABSTRACT
Aim To investigate the effect of acacetin on cell proliferation and the influence of acacetin on estrogen receptor expression in vitro.Methods The proliferation rates and the cell cycle changes of acace-tin-treated T47D cells were measured by sulforhodam-ine B(SRB)assay and flow cytometry,respectively. Moreover,the mRNA expressions of estrogen receptor-alpha(ERα),estrogen receptor-beta(ERβ)and pro-liferating antigen(Ki67)were determined by quantita-tive real time PCR (qPCR).Western blot was em-ployed to detect the ERαand ERβprotein expression. Results Acacetin significantly promoted the prolifera-tion and increased the amount of cells arrested in S and G2 /M phase under the concentration of 0.001 ~1 0μmol·L -1 .Ki67 mRNA level and the ERαprotein level in T47D cells were remarkably upregulated after acacetin treatment.To clarify which estrogen receptors played a role in acacetin induced the proliferation of T47D cells,the combination treatment of acacetin and ERαinhibitor (MPP)/ERβ inhibitor (PHTPP) was employed.We found that MPP could reverse the cell proliferation,the cell arrested in S and G2 /M phase and the increased Ki67 mRNA level induced by acace-tin.PHTPP also alleviated the T47D cell proliferation induced by acacetin,whereas no significant changes were found in cell cycle and Ki67 mRNA level.Con-clusion Acacetin stimulates the cell proliferation of T47D cells in the concentration from 0.001 μmol · L -1 to 1 0 μmol·L -1 ,which is mainly mediated by ERα.