Induction of autophagy by a novel small molecule improves aβ pathology and ameliorates cognitive deficits.

Growing evidence has demonstrated a neuroprotective role of autophagy in Alzheimer's disease (AD). Thus, autophagy has been regarded as a potential therapeutic target, attracting increasing interest in pharmaceutical autophagy modulation by small molecules. We designed a two-cycle screening strategy on the basis of imaging high-throughout screening (HTS) and cellular toxicity assay, and have identified a novel autophagy inducer known as GTM-1.

Quantitative proteomic study identified cathepsin B associated with doxorubicin-induced damage in H9c2 cardiomyocytes.

The study was performed to analyze the proteomic profiling of doxorubicin-treated H9c2 cardiomyocytes in order to identify novel protein biomarkers associated with doxorubicin-induced cardiomyopathy. The protein profiling of H9c2 cells in response to doxorubicin at an apoptosis-induced concentration of 0.5 μM were compared using iTRAQ analysis.

Inhibition of reactive oxygen species/extracellular signal-regulated kinases pathway by pioglitazone attenuates advanced glycation end products-induced proliferation of vascular smooth muscle cells in rats.

Advanced glycation end products (AGEs) have been shown to induce the proliferation of vascular smooth muscle cells (VSMCs) and contribute to atherogenesis and diabetes. In the present study, we investigated the effects of pioglitazone, a peroxisome proliferator activated receptor gamma (PPARγ) agonist, on AGE-induced rat VSMC growth and the underlying mechanism. In cultured rat VSMCs, AGE treatment induced VSMC proliferation in time- and dose-dependent manner, while down-regulated the expression of PPARγ.

Increased Siglec-1 expression in monocytes of patients with primary biliary cirrhosis.

Objectives: To evaluate Siglec-1 protein (CD169) and mRNA levels in peripheral blood monocytes of patients with primary biliary cirrhosis (PBC) and investigate its role in PBC pathogenesis by looking for correlations between Siglec-1 expression and key PBC associated biochemical indices.

Methods: FACS analysis was used to identify the percentage of peripheral blood monocytes positive for both CD14 and Siglec-1 in (a) 45 PBC patients, (b) 40 patients with liver cirrhosis after hepatitis B infection and (c) 36 healthy controls. Siglec-1 mRNA was measured by real-time RT-PCR and serum biomarkers by routine biochemistry.

Effects of methotrexate on plasma cytokines and cardiac remodeling and function in postmyocarditis rats.

Excessive immune activation and inflammatory mediators may play a critical role in the pathogenesis of chronic heart failure. Methotrexate is a commonly used anti-inflammatory and immunosuppressive drug. In this study, we used a rat model of cardiac myosin-induced experimental autoimmune myocarditis to investigate the effects of low-dose methotrexate (0.

The nonspecific anti-inflammatory therapy with methotrexate for patients with chronic heart failure.

Background: Inflammatory mediators play an important role in the pathogenesis of chronic heart failure (CHF). Methotrexate (MTX) is used in the treatment of inflammatory-mediated diseases (eg, rheumatoid arthritis) because it modulates the expression of numerous inflammatory cytokines. However, no studies have assessed the effects of MTX on plasma levels of inflammatory mediators in patients with CHF.

[Effect of shuxuetong in preventing restenosis after intracoronary stenting].

Objective: To evaluate the effect of shuxuetong (SXT) in preventing restenosis after intracoronary stenting.

Methods: Sixty-eight patients, accepted intracoronary stenting, were divided into two groups, the SXT group and the control group, both of them were treated with conventional treatment, and to the SXT group, SXT was given additionally. The condition of treated coronary artery restenosis in the two groups was compared by way of quantitative coronary angiography and a 6-month follow-up study was adopted.