Metformin Increases Cardiac Rupture After Myocardial Infarction via the AMPK-MTOR/PGC-1α Signaling Pathway in Rats with Acute Myocardial Infarction.

BACKGROUND Cardiac rupture often occurs after acute myocardial infarction due to complex and unclear pathogenesis. This study investigated whether metformin increases the incidence of cardiac rupture after myocardial infarction through the AMPK-MTOR/PGC-1α signaling pathway. MATERIAL AND METHODS An acute myocardial infarction (MI) mouse model was established. A series of experiments involving RT-qPCR, Western blot, TUNEL staining, and Masson staining were performed in this study. RESULTS Myocardial infarction occurred, resulting in the cardiac rupture, and the expression level of PGC-1α increased in the cardiac myocardium. Meanwhile, the proportion of myocardial NT-PGC-1α/PGC-1α decreased. The expression level of myocardial PGC-1α in MI mice with cardiac rupture after MI was significantly higher than that in the mice without cardiac rupture, and the ratio of myocardial NT-PGC-1α/PGC-1α was low. In addition, increasing the dose of metformin significantly increased the incidence of cardiac rupture after myocardial infarction in MI mice. High-dose metformin caused cardiac rupture in MI mice. Moreover, high-dose metformin (Met 2.0 nM) reduces the proportion of NT-PGC-1α/PGC-1α in primary cardiomyocytes of SD mice (SD-NRVCs [Neonatal rat ventricular cardiomyocytes]), and its effect was inhibited by Compound C (AMPK inhibitor). Further, after 3 days of treatment with high-dose metformin in MI mice, myocardial fibrin synthesis decreased and fibrosis was significantly inhibited. Meanwhile, cardiomyocyte apoptosis increased significantly. With the increase in metformin concentration, the expression level of myocardial LC3b gradually increased in MI mice, suggesting that metformin enhances the autophagy of cardiomyocytes. CONCLUSIONS These results suggest that metformin increases cardiac rupture after myocardial infarction through the AMPK-MTOR/PGC-1α signaling pathway.

Aqueous degradation of artificial sweeteners saccharin and neotame by metal organic framework material.

The artificial sweeteners (ASs) saccharin (SAC) and neotame (NEO) are widely used across the globe and are considered as emerging contaminants in surface, ground, and drinking waters. To degrade SAC and NEO, the metal organic framework material Co-based bio-MOF-11 was prepared by hydrothermal reaction and used with peroxymonosulfate (PMS) activator. The effects of the initial concentration of SAC and NEO, bio-MOF-11-Co dosage, PMS concentration, initial pH, temperature, and competitive anions were determined. The results revealed that bio-MOF-11-Co effectively catalyzed the degradation of SAC and NEO and possessed good stability and recycling efficiency. The degradation reaction was effective from pH 3.6-9.8 and followed quasi-first-order kinetics with degradation rate constants of 0.001-0.013 min-1 for SAC and 0.03-0.52 min-1 for NEO. Increased temperature was conducive to the degradation of both artificial sweeteners. The presence of Cl- inhibited the degradation of SAC and NEO, while the presence of CO32- promoted their degradation. Electron paramagnetic resonance (EPR) and free radical quenching demonstrated that the primary free radicals were sulfate radicals ( [Formula: see text] ) and hydroxyl radicals (HO). The change of cobalt oxidation state and electron transfer in bio-MOF-11-Co mainly induces the production of [Formula: see text] . A plausible mechanism for degradation is [Formula: see text] and HO attack on CS bonds, NS bonds, and benzene rings.

A Pyrene-functionalized Polynorbornene for Ratiometric Fluorescence Sensing of Pyrophosphate.

A novel pyrene-functionalized polynorbornene (P1) bearing sulfonamide NH and triazolium donors has been synthesized for ratiometric fluorescence sensing of PPi in aqueous solution. In addition, P1 is also used to monitor intracellular PPi and to detect PPi released during polymerase chain reaction.

Imaging and force measurement of LDL and HDL by AFM in air and liquid.

The size and biomechanical properties of lipoproteins are tightly correlated with their structures/functions. While atomic force microscopy (AFM) has been used to image lipoproteins the force measurement of these nano-sized particles is missing. We detected that the sizes of LDL and HDL in liquid are close to the commonly known values. The Young's modulus of LDL or HDL is ∼0.4 GPa which is similar to that of some viral capsids or nanovesicles but greatly larger than that of various liposomes. The adhesive force of LDL or HDL is small (∼200 pN). The comparison of AFM detection in air and liquid was also performed which is currently lacking. Our data may provide useful information for better understanding and AFM detection of lipoproteins.

A novel polynorbornene-based chemosensor for the fluorescence sensing of Zn2+ and Cd2+ and subsequent detection of pyrophosphate in aqueous solutions.

A hydroxyquinoline functionlized polynorbornene (P1) was designed and synthesized. In an aqueous solution, P1 shows a "turn-on" fluorescence response for Zn(2+) and Cd(2+) with a 50 nm blue shift. Furthermore, both P1-Zn(2+) and P1-Cd(2+) complexes were found to respond to pyrophosphate (PPi) over other important biological anions via a fluorescence quenching effect. P1 is also capable of monitoring intracellular Zn(2+) and PPi in real time.