ABSTRACT
Objective To investigate the protective effects of rhein lysinate ( RHL) on cardiac tissue damage in-duced by paraquat in experimental mice , and to clarify its mechanism .Methods In this study mice were assigned to the following three groups: control, paraquat model, and RHL-treated groups.The model of oxidative damage mice was established by intraperitoneal injection of paraquat .RHL-treated group was given RHL ( 50 mg/kg ) by gavage for one week before performing model .The other two groups were given equal volume of distilled water .For making model , paraquat was intraperitoneally injected in the paraquat model and RHL-treated group .The content of MDA was detected by thiobarbituric acid assay .The activities of SOD and GSH-Px were detected by biphenyl three phenolic autoxidation assay and NADPH coupling method respectivly .The pathological profile of cardiac tis-sue was observed by hematoxylin and eosin ( HE) staining and reactive oxygen species was observed by DCFH-DA staining .The change of proteins related to myocardial damage detected by Western blot .Results Compared with control group, the activities of SOD and GSH-Px decreased (P<0.05) and the content of MDA increased (P<0.05) in paraquat model group .However , these changes were attenuated byr RHL treatmen ( P<0.05 ) .The pathologi-cal examination indicated the structure of cardiac tissue was damaged and reactive oxygen species of cardiac tissue was increased after paraquat was given , however , these changes were attenuated after RHL treatmen .It was shown in western blot analysis that compared with control group , the expression of SIRT1 decreased, the acetylation of P53 and the expression of P 53 and P66 increased in paraquat-treated group .These changes were attenuated by RHL treatmen ( P<0.05 ) .Conclusions RHL may attenuate paraquat-induced cardiac injury in mice .
ABSTRACT
Objective To investigate the protective effect of rhein lysinate (RHL)on the liver of the models with diabetic rats,and to provide basis for research on treatment of fatty liver in the patients with diabetes mellitus. Methods The models of diabetic rats were established by intraperitoneally injecting streptozotocin(STZ).40 rats were divided into control,model,25 mg·kg-1 RHL,and 50 mg·kg-1 RHL groups(n=10).The levels of malonaldehyde (MDA)and the activities of superoxide dismutase (SOD)and glutathione peroxidase (GSH-Px) were detected by thiobarbituric acid method, pyrogallol autoxidation method, and NADPH coupling method, respectively.The pathological changes of liver tissue were observed by hematoxylin and eosin (HE)staining;the content of fat in liver tissue was observed by Nile red staining;the expression levels of fat synthesis-related proteins were detected by Western blotting method.Results Compared with control group,the body weight of the rats in model group was decreased and the levels of blood glucose,total cholesterol(TC)and triglyceride(TG)were increased (P<0.05);the activities of SOD and GSH-Px in liver tissue were decreased (P<0.05);there were a plenty of fat vacuoles and fat accumulation in liver tissue. The signal pathway of fat synthesis-related ERK1/2-SREBP-1c was activated in model group;compared with model group,it was inhibited in 25 and 50 mg· kg-1 RHL groups (P<0.05).Compared with model group,the blood glucose,TC and TG of the rats in 25 and 50 mg ·kg-1 RHL groups were decreased (P<0.05);the activities of SOD and GSH-Px were increased (P<0.05);however the body weight had no change. Compared with model group, the fatty vacuoles and the fatty accumulation of liver tissue in 25 and 50 mg·kg-1 RHL groups were decreased. Conclusion The hepatic protection of RHL is correlated with the inhibition of oxidative stress, fat degeneration and fatty accumulation of liver tissues.
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Objective To detect the expression levels of the miR-205 in lung cancer tissue and A549 cells and its targeted gene YES1 using qRT-PCR and dual fluorescence protein repoter assay system,and to explore the possible mechanism of miR-205 to inhibit the proliferation of lung cancer A549 cells.Methods The expression levels of miR-205 in 10 cases of lung cancer tissue and adjacent normal lung tissue were detected with qRT-PCR.The cell growth curve and colony formation assay were used to determine the proliferation rate of A549 cells after transfected by miR-205 mimics and control mimics.The sequences of YES1 3′UTR (untranslated region)and mutation target sites of YES1 3′UTR were inserted into the plasmid which expressed green fluorescence protein (pcDNA3/EGFP) respectively to construct the green fluorescence protein plasmids of YES1-3′UTR and mut-YES1-3′UTR. There were six groups in the study:YES1-3′UTR, YES1-3′UTR and miR-205 mimics, YES1-3′UTR and control mimics,mut-YES1-3′UTR, mut-YES1-3′UTR and miR-205 mimics, mut-YES1-3′UTR and control mimics;after the plasmids expressed red fluorescent protein (pDsRed2-N1 )were cotransfected into A549 cells,the extracted protein was detected with fluorescence spectrophotometer.Results Compared with adjacent normal lung tissue,the expression levels of miR-205 in lung cancer tissue and A549 cells were decreased (P<0.05 );the proliferation rate of A549 cells in miR-205 mimics group was lower than that in control mimics group (P<0.05). The fluorescence protein expression level in YES1-3′UTR and miR-205 mimics co-transfected group was lower than that in YES1-3′UTR and control mimics co-transfected group, the difference was statistically significant (P<0.01).The number of cell colony formation of A549 cells in highly expressed YES1 group was higher than that in cell control group (P<0.05).Conclusion MiR-205 may inhibit the proliferation of A549 cells through regulating of the expression of YES1 directly.miR-205 and YES1 are potential therapeutic targets for the biological treatment of tumor.