Valsartan improves cardiac function in mice with diabetes mellitus by CaMKII/AngII.

OBJECTIVE: To investigate whether valsartan exerts its effect on cardiac function in mice with diabetes mellitus (DM) via Ca2+/calmodulin-dependent protein kinase II (CaMKII). MATERIALS AND METHODS: C57bl6/J mice were used as study subjects and randomly divided into three groups: 1) control group, 2) DM group and 3) valsartan group. After the model was successfully established, the diastolic function in each group of mice was detected via echocardiography, including the ratio of peak velocity blood flow in early diastole to peak velocity blood flow in late diastole (E/A ratio) of mitral valves, isovolumic relaxation time (IVRT) and mitral deceleration time. Ejection fraction (EF), fractional shortening (ES), heart rate (HR) and cardiac output (CO) were determined to evaluate the systolic function of the mouse heart. The frozen heart was stained by dihydroethidium (DHE) and analyzed for the oxidative stress and inflammation levels. The expression levels of phosphorylated calmodulin-dependent protein kinase II (P-CaMKII), oxidized CaMKII (O-CaMKII), ryanodine receptor 2 (RYR2), P-phospholamban (P-PLN) and PLN in tissues were detected via Western blotting. RESULTS: Valsartan improves myocardial diastolic and systolic function in DM mice by improving phosphorylation and oxidation levels of CaMKII in myocardial cells, and reducing oxidative stress in diabetic cardiomyopathy. CONCLUSIONS: Valsartan could improve CaMKII in myocardial cells to enhance oxidative stress of DM mice, thus improving the cardiac function.

AMPK regulates energy metabolism through the SIRT1 signaling pathway to improve myocardial hypertrophy.

OBJECTIVE: We investigated the correlations of adenosine monophosphate-activated protein kinase (AMPK), Silence information regulator 1 (SIRT1) and energy metabolism with myocardial hypertrophy. MATERIALS AND METHODS: Myocardial hypertrophy experimental model was established via transverse aortic constriction (TAC)-induced myocardial hypertrophy and phenylephrine (PE)-induced hypertrophic myocardial cell culture. After activation of AMPK, the messenger ribonucleic acid (mRNA) expressions in myocardial tissue- and myocardial cell hypertrophy-related genes, atrial natriuretic peptide (ANP) and ß-myosin heavy chain (ß-MHC), were detected. The production rate of 14C-labeled 14CO2 from palmitic acid was quantitatively determined to detect the fatty acid and glucose oxidation of hypertrophic myocardial tissues or cells, and the glucose uptake of myocardial cells was studied using [14C] glucose. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were performed to detect the changes in SIRT1 mRNA and protein expressions in hypertrophic myocardial tissues. Moreover, SIRT1 small interfering ribonucleic acid (siRNA) was used to interfere in SIRT1 expression to further investigate the role of SIRT1 in the effect of AMPK activation on myocardial hypertrophy. RESULTS: AMPK activation could significantly reduce the mRNA expressions of ANP and ß-MHC in vitro and in vivo. AMPK could increase the ejection fraction (EF) and decrease the protein synthesis rate in myocardial cells in mice with myocardial hypertrophy. Besides, AMPK activation could increase the fatty acid oxidation, improve the glucose uptake and reduce the glucose oxidation. After AMPK activation, both SIRT1 mRNA and protein expressions in hypertrophic myocardial tissues and myocardial cells were increased. After SIRT1 siRNA was further used to interfere in SIRT1 expression in myocardial cells, it was found that mRNA expressions and protein synthesis rates of ANP and ß-MHC were increased. CONCLUSIONS: The activation of AMPK can inhibit the myocardial hypertrophy, which may be realized through regulating the myocardial energy metabolism via SIRT1 signaling pathway.

Clinical efficacy of fiberoptic ductoscopy in combination with ultrasound-guided minimally invasive surgery in treatment of plasma cell mastitis.

OBJECTIVES: To analyze clinical efficacy between fiberoptic ductoscopy plus ultrasound-guided minimally invasive irrigation and lesion resection in treating plasma cell mastitis (PCM), aiming to provide clinical evidence for treating PCM. MATERIALS AND METHODS: 119 patients undergoing fiberoptic ductoscopy plus ultrasound-guided minimally invasive surgery in Ningxia People's Hospital were allocated into the breast duct irrigation group, and 95 counterparts receiving lesion resection in the Affiliated Hospital of Ningxia Medical University into the control group. Clinico-pathological characteristics and therapeutic effect were compared between two groups. RESULTS: The cure rate in the breast duct irrigation group was 98.31% (117/119), significantly higher than 90.53% in the control group (p < 0.05). In the breast duct irrigation group, overall treatment time was 20.13 days, significantly longer than 15.15 days in the control group (p < 0.05). During postoperative follow-up, no recurrence was observed, significantly lower compared with 48.8% (42/86) in the control group. The degree of satisfaction in the breast duct irrigation group was 95.79% (114/119), significantly higher compared with 74.74% (71/95) in the control group. CONCLUSIONS: Fiberoptic ductoscopy plus with ultrasound-guided minimally invasive drainage is a novel and effective treatment of PCM with high cure rate, low recurrence rate, slight pain, and effectively maintains breast integrity.