Protective effects of antioxidants on chronic intermittent hypoxia-induced cardiac remodeling in mice / 中华心血管病杂志

<p><b>OBJECTIVE</b>Chronic intermittent hypoxia (CIH) animal model was used to mimic the status of obstructive sleep apnea (OSA) in order to investigate the pathological mechanism of CIH-induced cardiac remodeling and observe the protective effect of antioxidants.</p><p><b>METHODS</b>FVB mice (8-10 weeks-old) were randomly divided into control (saline, i.p.) group and CIH group, reduced form of nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin (APO, 3 mg×kg(-1)×d(-1), i.p.) alone or CIH+APO, SOD mimic MnTMPyP (SODM, 5 mg×kg(-1)×d(-1), i.p.) alone or CIH+SODM (n = 5 each). After 4 weeks, cardiac function and structure were determined by echocardiography, cardiac inflammation, apoptosis, cardiac fibrosis and cardiac MDA contents were examined by Western blot and chemical-biological methods, respectively.</p><p><b>RESULTS</b>(1) Heart weight, LVIDd and LVIDs were increased while LVEF and FS were reduced in CIH group compared to control group (all P < 0.05). (2) Myocardial protein expression of ANP and VCAM-1 was significantly upregulated, myocardial MDA content and apoptosis as well as myocardial fibrosis marker CTGF and PAI-1 were increased in CIH group compared to control group (all P < 0.05). (3) Above parameters were similar between APO and CIH+APO as well as SODM and CIH+SODM (all P > 0.05).</p><p><b>CONCLUSION</b>CIH could induce cardiac remodeling and CIH-induced cardiac inflammation, cardiac oxidative injury, cardiac apoptosis and cardiac fibrosis serve as the pathological mechanisms of CIH-induced cardiac remodeling. The protective effects of the two antioxidants suggest that the main mechanism of CIH-induced cardiac injury is oxidative stress.</p>

The effeot of trimetazionshe hydnchlorile Tabletsand compatite seolora brokkig in treahig wngethe heat failure / 中国实用内科杂志

Objective To discuss effects of Trimetazidine Dihydrochloride Tablets and Composite Saliviae Dropping Pill in treating congetive heart failure.Methods 191 patients of congestive heart failure were randomly divided into the treatment group(n=96)and the control group(n=95).The treatment group based on therapy as the control group adds Trimetazidine Dihydrochloride Tablets(20 mg,three time per day,by mouth)and Composite.Saliviae Dropping Pill(15 grains every time,three times per day,hy mouth).The control group was treated with Aspirin,?-retarder, ACEI,diuresis,and tonify the heart and blood vessel activity drug.Results 49 patients(51.0%)were apparent, and 40 patients were effective in treatment group(41.7%),the total effective rate was92.7%; the control group's were apparent 39 patients(41.1%)were apparent,and 37 patients(38.9%)were effective in control group,the total ef- fective rate was 80.0%.The total effctive rate of two groups according to statistics(x~2=6.56,P

Thymosin ?_4 raises survival rate and down-regulatesinflammatory mediators in septic shock mice / 重庆医科大学学报

Objective:To explore the mechanism of action of thymosin ? 4 (T? 4) in septic shock by observing the 72h survival rate of septic shock mice treated with thymosin ? 4 and exploring the changes of TNF-? and IL-1?.Methods:LPS(lipopolysaccharide) was intraperitoneally injected into clean Kunming mice to establish the animal model.①The T? 4,between normal and septic shock mice were determined.②The survival rate of septic shock mice was studied by intraperitoneal injection of T? 4.Animals were divided into four groups of 30 and each received LPS(25mg/kg)intraperitoneal injection.Group Ⅰ was LPS control group.GroupⅡ,Ⅲ and Ⅳ were individually injected with T? 4 at 0h,0h,2h;0h,2h,4h post LPS through caudal vein.③TNF-? and IL-1? were examined in septic shock mice by ELISA.Results:T? 4 was obviously decreased in the blood of septic shock mice.T? 4 could raise the 72h survival rate of septic shock mice and down-regulate inflammatory mediators.Conclusion:The optimal protective methods in the mouse appears to be 5mg/kg T? 4 given immediately following(0h) and at 2h and 4h successively post LPS.T? 4 down-regulates the inflammatory mediators,which may be the mechanism of T? 4 in curing the septic shock.