All the animal groups received an injection of 5 mg/kg MTX. Malonyldialdehyde (MDA), myeloperoxidase (MPO), gluthation (GSH), glutatione peroxidase (GPx) and superoxide dismutase (SOD) levels in the cerebrum tissue were measured. The experiment results of MDA, MPO, GSH, GPx and SOD levels in the brain tissue of the methotrexate group were 13.8 +/- 2.9 mu mol/g protein, 18.1 +/- 3.4 u/g protein, 4.1 +/- 1.1 nmol/g protein, 4.8 +/- 1.4 u/g protein and 6.8 +/- 1.5 u/g protein, respectively, while the values in the thiamin group were 12.6 +/- 2.5 mu mol/g protein, 17.1 +/- 3.5 u/g protein, 4.5 +/- 1.2

nmol/g protein, 5.6 +/- 2.1 u/g protein and 8.0 +/- 2.4 u/g protein, respectively. The levels in the TPP group for the same parameters were 5.0 +/- 0.5 mu mol/g protein, 6.4 +/- 0.8u/g protein, 8.1 +/- 0.5 nmol/g protein, 11.2 +/- 0.7 u/g protein and 15.6 +/- 1.5 u/g protein, respectively. In the control group, they SRT1720 in vivo were determined as 4.4 +/- 0.8 mu mol/g protein, 5.8 +/- 1.1 u/g protein, 9.8 +/- 2 nmol/g protein, 12.8 +/- 1.9 u/g protein and 18.8 +/-

2.5 u/g protein, respectively. TPP was found to have prevented the increase in MDA and MPO levels, and to have prevented the decrease in GSH, GPx and SOD levels by methotrexate, while thiamine did not. These findings suggested that methotrexate may be a thiamine antimetabolite.”
“Background: Myocardial fibrosis plays a critical role in heart failure, resulting in cardiac structural and electrical find more remodeling which can induce atrial arrhythmias. Collagen is the major element of fibrosis. However, it is not clear whether collagen can directly regulate the calcium homeostasis and the electrophysiologic characteristics of cardiomyocytes. The aim of this study was to determine the effects of collagen on calcium homeostasis and the electrical properties of atrial cardiomyocytes.

Methods and Results: HL-1 cardiomyocytes were cultured with and without collagen type I (1 or 10 mu g/mL) or losartan (10 mu mol/L). Whole-cell clamp, indo-1 fluorescence, and Western blotting were used to evaluate the action potential (AP) and ionic currents, intracellular calcium homeostasis, and calcium regulatory proteins. Compared

with the control samples, there was no significant difference in collagen (1 mu g/mL) treated HL-1 Selleckchem FDA-approved Drug Library cardiomyocytes. However, collagen (10 mu g/mL) treated HL-1 cardiomyocytes exhibited larger intracellular calcium ([Ca(2+)](i)) transients by 113% and a larger sarcoplasmic reticulum calcium content by 86%. Collagen (10 mu g/mL) treated HL-1 cardiomyocytes had higher expression of sarcoplasmic reticulum ATPase (SERCA2a) and Thr17-phosphorylated phospholamban but similar protein expressions of the Na(+)/Ca(2+) exchanger and ryanodine receptor. Collagen (10 mu g/mL) treated HL-1 cardiomyocytes (n = 11) had larger AP amplitude (104 +/- 5 vs 83 +/- 7 mV; P < .05), and shorter 90% of AP duration (25 +/- 2 vs 33 +/- 2 ms, P < .05) than control cells (n = 11).