Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway

Purpose: To investigate the protective role of tectorigenin in myocardial ischaemia/reperfusion. Methods: Myocardial cells (H9c2) were treated with different concentrations of tectorigenin and exposed to hypoxia/reoxygenation. Cell viability and apoptosis were determined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) staining, respectively. Oxidative stress and inflammation were evaluated using enzyme-linked immunosorbent assay (ELISA), while autophagy and the underlying mechanisms of action were evaluated by Western blot. Results: Tectorigenin enhanced the proliferative activity of H9c2 under hypoxia/reoxygenation conditions, and significantly reduced the apoptotic activity (p < 0.001) through decrease in Bax and increase in Bcl-2. Tectorigenin also significantly up-regulated SOD (superoxide dismutase) and GSH (glutathione) levels (p < 0.01), and down-regulated MDA (malondialdehyde) and MPO (myeloperoxidase) in hypoxia/reoxygenation-induced H9c2. TNF-α (tumor necrosis factor-α), IL(interleukin)-1β, and IL-6 levels were also inhibited by tectorigenin by down-regulating p-p65. Hypoxia/reoxygenation-induced increase in p62 and decrease in Beclin-1 and LC3-II/LC3-I were reversed by tectorigenin. Protein expressions of p-mTOR, p-AKT, and p-PI3K in hypoxia/reoxygenation-induced H9c2 were elevated by tectorigenin. Conclusion: Tectorigenin exerts anti-oxidant, anti-inflammatory, and anti-autophagic effects on hypoxia/reoxygenation-induced H9c2 through the activation of PI3K/AKT/mTOR pathway, thus suggesting that it is a potential agent for the management of myocardial ischaemia/reperfusion

Robust Transceiver with Tomlinson-Harashima Precoding for Amplify-and-Forward MIMO Relaying Systems

In this paper, robust transceiver design with Tomlinson-Harashima precoding (THP) for multi-hop amplify-and-forward (AF) multiple-input multiple-output (MIMO) relaying systems is investigated. At source node, THP is adopted to mitigate the spatial intersymbol interference. However, due to its nonlinear nature, THP is very sensitive to channel estimation errors. In order to reduce the effects of channel estimation errors, a joint Bayesian robust design of THP at source, linear forwarding matrices at relays and linear equalizer at destination is proposed. With novel applications of elegant characteristics of multiplicative convexity and matrix-monotone functions, the optimal structure of the nonlinear transceiver is first derived. Based on the derived structure, the transceiver design problem reduces to a much simpler one with only scalar variables which can be efficiently solved. Finally, the performance advantage of the proposed robust design over non-robust design is demonstrated by simulation results.Comment: IEEE Journal on Selected Areas in Communications - Special Issue on Theories and Methods for Advanced Wireless Relays The final version and several typos have been correcte

Research progress of MicroRNA in podocytes autophagy in diabetic nephropathy

Diabetic nephropathy (DN) is one of the most common microvascular complications of diabetes, and is a kind of abnormal microangiopathy of kidney structure, function or clinical indicators caused by diabetes. Podocyte injury has been considered as a major contributor to the progression of diabetic nephropathy(DN). microRNA can participate in podocytes injury through autophagy.In this paper, the mechanism of microRNA involved in DN podocytes autophagy was reviewed to provide reference for the treatment of DN in the future