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AIM:To explore the changes of plasma levels of soluble vascular endothelial growth factor receptor 2 ( sVEGFR2) and superoxide dismutase ( SOD) in hypertensive patients and hypertensive diabetic patients.METHODS:In this cross-sectional study, 88 cases were enrolled, which were divided into hypertensive group (n=31), hypertensive diabetic group ( n=31 ) and control group ( n=26 ) .Blood pressure was obtained from each participant with mercury sphygmomanometer.The levels of sVEGFR2 and SOD were measured by ELISA.Meanwhile, the levels of plasma glucose, glycosylated hemoglobin A1c ( GHbA1c) and lipid profile were detected.RESULTS:The levels of total cholesterol ( TC) and body mass index (BMI) were significantly higher in hypertensive group than those in control group (P<0.05).The levels of TC, low-density lipoprotein cholesterol ( LDL-C) , triglyceride ( TG) , BMI, waist circumference were significantly higher in hypertensive diabetic group than those in control group (P<0.05).The plasma levels of sVEGFR2 and SOD in both hypertensive diabetic group and hypertensive group were significantly decreased compared with control group ( P<0.05), while the mean plasma levels of sVEGFR2 and SOD in hypertensive diabetic group were significantly decreased compared to the hypertensive group ( P<0.05 ) .A significantly positive correlation between sVEGFR2 and SOD in the whole study population (P<0.05) was observed.CONCLUSION: The plasma level of sVEGFR2 is decreased in both hypertensive and hypertensive diabetic patients, and more significantly decreased in hypertensive diabetic patients.De-creased SOD level may be associated with to the reduction of sVEGFR2.
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AIM: To explore the effect of hydrogen sulfide on the senescence of human umbilical vein endothe -lial cells (HUVECs) induced by high glucose.METHODS: Senescence model was established by treating HUVECs with33 mmol/L glucose for 48 h.The parameters were detected to demonstrate the effect of hydrogen sulfide on senescence andthe mechanism involved was also investigated .RESULTS: In the cells treated with high glucose, the proliferation was attenuatedwith a higher number of senescence -associated β-galactosidase (SA-β-Gal) positive cells, and plasminogen activatorinhibitor 1 (PAI-1) protein expression, malondialdehyde (MDA) production and NF-κB p65 activity were increasedsignificantly, but the expression of superoxide dismutase 1 (SOD1) was decreased.However, the cell number and SOD1expression were increased, and the number of SA-β-Gal positive cells, PAI-1 protein expression, MDA production and theactivity of NF-κB p65 were decreased after sodium hydrosulfide (100 and 200 μmol/L) treatment.CONCLUSION: Exogenoushydrogen sulfide prevents HUVECs against high glucose -induced senescence by suppressing oxidative stress and NF -κB p65 activity.
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OBJECTlVE To investigate the myocardiaI toxicity of doxorubicin on the myocardium of rabbits and mechanism. METHODS Doxorubicin 2 mg·kg-1 was injected once a week for eight weeks. After discontinuation of doxorubicin,observation was performed for another 8 weeks. Every weekend, uItrasound examination,cardiac catheterization,angiotensinⅡ(AngⅡ)Western bIotting and pathoIogi-caI examination were performed to anaIyze eject fraction( EF),maximaI rate of rise of Ieft ventricuIar pressure(+dp/ dtmax ),AngⅡexpression IeveI,apoptosis index(AI)and the structure of the myocardium. RESULTS At the 7th injection,EF decreased( P ﹤0.05),but reached the bottom vaIue at the 8th injection. At the 3rd injection,Ieft ventricuIar +dp/ dtmax decreased( P ﹤0.05)and reached the bottom vaIue one week after withdrawaI. After that,it increased and reached a high vaIue six weeks after withd-rowaI. But it was stiII Iower than before administration. At the 2nd injection,AngⅡ expression increased (P﹤0.05). At 1 week after withdrawaI,it reached the top vaIue,but than decreased and reached a Iow vaIue six weeks after withdrowaI,but was stiII higher than before administration. At the 1st injection,AI increased( P ﹤ 0.05). At 1 week after withdrawaI,it reached the top vaIue,but then decreased and reached a Iow vaIue 5 weeks after withdrawaI. But it was stiII higher than before administration. CONCLUSlON Doxorubicin cardiac toxicity can induce an eIevated IeveI of myocardiaI AngⅡ,possibIy associated with increased aIdosterone and myocardiaI tension. Increased Ang Ⅱ may induce further myocardiaI structuraI damage and ventricuIar remodeIing through the ROS and caIcium imbaIance.