Objective: To investigate the correlation between serum melatonin level and cardiac function, blood lipid in patients of heart failure with preserved ejection fraction (HFpEF). Methods: One hundred and seventy patients with HFpEF (HFpEF group) in Ninth Hospital of Xi′an City from May 2016 to May 2018 were selected. According to the cardiac function grading of New York Heart Association (NYHA), Ⅱ grade (cardiac function Ⅱ grade) was in 98 cases, and Ⅲ grade (cardiac function Ⅲ grade) was in 72 cases. Then, 32 healthy volunteers were selected as control group. The 2 groups were sampled at 2:00 and 7:00, and the level of melatonin was detected by enzyme-linked immunosorbent assay. The correlation between serum melatonin level and cardiac function, blood lipid were analyzed (Pearson correlation), including triglyeride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), N-terminal precursor brain natriuretic peptide (NTproBNP), hypersensitive C reactive protein (hs-CRP), ejection fraction, left ventricular end-diastolic volume index (LVEDVI), miral diastolic early and end-diastolic maximum blood flow velocity ratio (E/A) and peak value of early diastolic blood flow velocity in the mitral valve and peak value of the early diastolic velocity of the mitral annulus (E/e′). Results: The TG, TC, LDL-C, NTproBNP and hs-CRP in cardiac function Ⅲ grade patients were significantly higher than those in cardiac function Ⅱ grade patients: (1.51 ± 0.69) mmol/L vs. (1.15 ± 0.75) mmol/L, (4.03 ± 1.02) mmol/L vs. (3.47 ± 0.94) mmol/L, (1.42 ± 0.33) mmol/L vs. (1.17 ± 0.31) mmol/L, (3 438.54 ± 553.58) ng/L vs. (3 034.58 ± 557.35) ng/L and (4.26 ± 2.54) mg/L vs. (3.12 ± 2.13) mg/L, the HDL-C, ejection fraction and E/A were significantly lower than those in cardiac function Ⅱ grade patients: (2.44 ± 0.88) mmol/L vs. (2.97 ± 0.94) mmol/L, (56.23 ± 5.26)% vs. (61.11 ± 5.33)% and 0.82 ± 0.18 vs. 0.91 ± 0.17, and there were statistical differences (P<0.01). The melatonin levels at 2:00 and 7:00 in control group and cardiac function Ⅱgrade patients of HFpEF group were significantly higher than those in cardiac function Ⅲ grade patients of HFpEF group: (454.24 ± 123.54) and (432.68 ± 155.68) ng/L vs. (368.85 ± 98.52) ng/L, (483.25 ± 90.54) and (418.54 ± 103.57) ng/L vs. (345.85 ± 98.52) ng/L, the melatonin level at 7:00 in control group was significantly higher than that in cardiac function Ⅱ grade patients of HFpEF group, and there was statistical difference (P<0.01). In cardiac function Ⅱ grade patients of HFpEF group, the melatonin level was correlated with TG, TC, LDL-C and HDL-C (P<0.01); In cardiac function Ⅲ grade patients of HFpEF group, the melatonin level was correlated with NTproBNP, hs-CRP, ejection fraction, LVEDVI, E/A, E/e′, TG, TC, LDL-C and HDL-C (P<0.01 or <0.05). Conclusions The melatonin level is correlated with the level of blood lipid in HFpEF patients. Melatonin level is correlated with cardiac function Ⅲ grade patients, but this phenomenon is not observed in cardiac function Ⅱ grade patients.

【Objective】 To evaluate the effects of miR-148a-3p on calreticulin (CRT) expression and mitochondrial function in cardiomyocytes incubated with high glucose. 【Methods】 miR-148a-3p minic and inhibitor were used to intervene the H9c2 cardiomyocytes of rats. The expression of CRT protein was detected. Then the cells were divided into control group, high-glucose group (HG), HG +miR-148a-3p minic group, HG + miR-148a-3p minic + TG (CRT agonist) group, HG + miR-148a-3p inhibitor group, and HG + miR-148a-3p inhibitor + CRT- (CRT-siRNA) group. The content of adenosine triphosphate (ATP) and the level of reactive oxygen species (ROS), the activity of mitochondrial respiratory chain complex enzyme and apoptotic rate were detected. 【Results】 miR-148a-3p minic significantly inhibited the expression of CRT protein in cardiomyocytes, while miR-148a inhibitor increased the expression of CRT. miR-148a-3p minic inhibited the decrease of ATP production, the increase of ROS production and cell apoptosis, and the inactivity of mitochondrial respiratory chain complex enzyme in cardiomyocytes induced by high glucose, while TG weakened the above effects of miR-148a-3p minic. miR-148a inhibitor aggravated the mitochondrial injury and apoptosis of cardiomyocytes induced by high glucose, but the effects of miR-148a-3p inhibitor were partially blocked by CRT-siRNA. 【Conclusion】 miR-148a-3p negatively regulates the expression of CRT in cardiomyocytes and protects the mitochondrial injury and apoptosis induced by high-glucose through inhibiting CRT.