ABSTRACT
Objective:To observe the effect of selenium supplementation on 10-year survival rate of chronic Keshan disease (KD).Methods:The 10-year follow-up data of 302 patients with chronic KD at the KD surveillance sites in Shaanxi Province were collected from the Shaanxi Institute for Endemic Disease Control and Research and Xi'an Jiaotong University, 170 (56.3%) cases were given selenium supplementation (oral administration of sodium selenite tablet, once a week, 1 mg/time) until the end point of follow-up as selenium supplementation group, and the rest (132 cases) were non-selenium supplementation group. Cox proportional hazards models were used to identify the independent predictors for 10-year survival rate of chronic KD. Kaplan-Meier method was used to analyze the 10-year survival rate of patients with chronic KD during the follow-up period and the Log-rank test was used to compare the 10-year survival rate between groups.Results:The follow-up deadline was October 2019. During the follow-up period, a total of 199 patients (199/302, 65.9%) of chronic KD died, including 101 patients (101/170, 59.4%) in the selenium supplementation group and 98 patients (98/132, 74.2%) in the non-selenium supplementation group. In COX proportional hazards model, after adjustment for other baseline characteristics [age, sex, body mass index (BMI), family history of KD, smoking, blood pressure, heart rate, ECG abnormalities, initial cardiothoracic ratio, left ventricular ejection fraction (LVEF), and blood selenium content], selenium supplementation and combined use of angiotensin-converting enzyme inhibitor + β receptor blocker (ACEI + BBs) were protective factors for 10-year survival in patients with chronic KD (selenium supplementation: HR = 0.39, 95% CI: 0.28 - 0.53; ACEI + BBs: HR = 0.57, 95% CI: 0.39 - 0.84). The 10-year survival rate of chronic KD patients after selenium supplementation was significantly higher than that of non-selenium supplementation group (Log-rank test, P < 0.05). Conclusion:Selenium supplementation and combined use of ACEI + BBs in chronic KD patients, are associated with better survival during the 10-year follow-up.
ABSTRACT
Objective To explore the changes of cardiac structure and function in streptozotocin (STZ)-induced diabetic cardiomyopathy (DCM)rats so as to detect the level of angiotensinⅡ (AngⅡ)in blood and the myocardium and illuminate the role of AngⅡ in DCM.Methods We randomly divided 30 SD rats into control group and DCM group (which received a single injection of streptozotocin,65 mg/kg).The changes of cardiac structure and function were observed by ultrasonic cardiogram at the end of 16 weeks after injection.Then the changes in the myocardium were also analyzed by using hemotoxylin and eosin staining and Sirius red staining.The level of AngⅡ in blood was tested by radioimmunoassay.The expression of AngⅡ in the myocardium was detected by immunofluorescence. Results Compared with those of the controls,the hearts were dilated in DCM rats accompanied with cardiac dysfunction.There were significant increases in LVEDd,LVESd,LVEDv,and LVESv but decrease in LVEF (P <0.05).There were arrangement disorder and hypertrophic cardiomyocytes in DCM.Then the fibrosis area of DCM was significantly increased compared with that of the controls.The level of AngⅡ in blood and myocardium was significantly higher in DCM than in controls.At the same time,Pearson analysis revealed that the level of AngⅡ in blood was positively related to the collagen content of myocardium (r =0.907,P <0.05).Conclusion Our study provides experimental evidence that AngⅡ plays an important role in myocardial fibrosis of DCM.
ABSTRACT
[ ABSTRACT] AIM:To observe the effect of high glucose on the protein expression of calreticulin ( CRT) and its association with cell apoptosis and mitochondrial dysfunction in the cardiomyocytes.METHODS: AC-16 cardiomyocytes were randomly divided into normal glucose group, high glucose group, high glucose+CRT siRNA group and isotonic con-trol group.The cell apoptotic rate, reactive oxygen species (ROS), mitochondrial membrane potential level, respiratory enzyme activity, and protein expression of CRT were observed.RESULTS: Compared with the cardiomyocytes in normal glucose group, the apoptotic rate and ROS production of cardiomyocytes increased in high glucose group, accompanying with the decreases in the mitochondrial membrane potential level and enzyme activitiy of the respiratory chain.The protein expression of CRT was significantly increased in high glucose group.However, compared with high glucose group, high glucose+CRT siRNA decreased the expression of CRT and attenuated the damage of mitochondria, but CRT siRNA did not reduce the ROS level in cardiomyocytes.CONCLUSION:High glucose brings about CRT over-expression to induce mito-chondrial injury, thus increasing myocardial apoptosis.
ABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of angiotensin II (Ang II) on calreticulin (CRT) expression and its association with mitochondrial dysfunction in cardiomyocytes.</p><p><b>METHODS</b>Primary neonatal rat cardiomyocytes were randomly divided into CRT siRNA group, control siRNA group, control group, Ang II+ CRT siRNA group, Ang II+ control siRNA group and Ang II group. The cell surface area, protein synthesis rate, mitochondrial membrane potential level, enzyme activities, and CRT expression were observed.</p><p><b>RESULTS</b>Compared with those in the control group, the cell surface area and protein synthesis rate were both increased and mitochondrial membrane potential level and enzyme activities decreased in Ang II groups. CRT expression was significantly down-regulated in Ang II+ CRT siRNA group with increased cell surface area, protein synthesis rate, mitochondrial membrane potential level and enzyme activities as compared with those in Ang II+ control siRNA group.</p><p><b>CONCLUSION</b>Ang II up-regulates CRT expression to induce mitochondrial injury, which may be an important mechanism of myocardial hypertrophy.</p>
Subject(s)
Animals , Rats , Angiotensin II , Pharmacology , Calreticulin , Metabolism , Cardiomegaly , Cells, Cultured , Membrane Potential, Mitochondrial , Mitochondria , Pathology , Myocytes, Cardiac , Pathology , Protein Biosynthesis , RNA, Small InterferingABSTRACT
<p><b>OBJECTIVE</b>To study the phosphorylation activity of mitochondrial signal transducer and activator of transcription 3 (STAT3) in the myocardium of rats with selenium deficiency and its association with myocardial injury.</p><p><b>METHODS</b>Thirty-six rats were randomized into normal control group (n=18) and selenium deficiency model group (n=18) for feeding with normal and low-selenium chow, respectively, for 20, 30 and 40 weeks. The cardiac function of the rats was evaluated by carotid artery intubation, and the damage of cardiac mitochondria was observed under electron microscopy. The cardiac mitochondria were extracted for assessing succinate dehydrogenase and cytochrome C oxidase activities, and the protein expressions of phosphorylated and total STAT3 were detected.</p><p><b>RESULTS</b>Compared with the corresponding control groups, the rats in the model group showed significantly decreased cardiac function with obvious structural and functional damage of the cardiac mitochondria (P<0.05), which aggravated as the low-selenium feeding time extended (P<0.05). The rats in the model group also showed significantly decreased mitochondrial STAT3 activity (p-STAT3/STAT3) in the myocardium as the low-selenium feeding time prolonged (P<0.05). Pearson linear correlation analysis showed that the activity of cardiac mitochondrial STAT3 had positive correlations with the left ventricular systolic pressure, maximal increased rate of the left ventricular pressure, and the activities of succinate dehydrogenase and cytochrome C oxidase (P<0.01).</p><p><b>CONCLUSION</b>Selenium deficiency down-regulates the activity of mitochondrial STAT3 in rat heart to contribute to cardiac mitochondrial injury and the progression of heart failure.</p>