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

Modulación del metabolismo postcosecha de glucosinolatos en maca (Lepidium meyenii)

La maca es una planta nativa andina que se cultiva sobre los 4000 m.s.n.m. en Junín y Pasco (Perú) y que es utilizada como alimento o medicina tradicional desde tiempos precolombinos. Este tubérculo ha sido objeto de numerosos estudios y se ha confirmado su alto valor nutricional y energizante ya que se han identificado ecompuestos bioactivos en maca tales como bencilglucosinolato, bencilisocianato y alcamidas benciladas. Este último grupo de compuestos, alcamidas benciladas, tienen un papel estimulatorio en el sistema nervioso central y son marcadores de actividad biológica en esta raíz ya que solo se les ha reportado en ella. Por este motivo se les denominó macamidas. Estudios previos han confirmado que no existen macamidas en maca fresca. Se determinó que la formación de macamidas ocurre exclusivamente durante el proceso de secado. Esparza y colaboradores (2015) estudiaron la cinética de su formación realizando experimentos de secado en campo durante nueve semanas e imitando el proceso en laboratorio en 24 horas en los que se identificaron y monitorearon los metabolitos precursores de las macamidas y, de este modo, se pudo plantear una vía tentativa que lleva a su acumulación. En el presente trabajo, se buscó conocer de manera más detallada las vías degradativas de glucosinolatos durante el proceso de secado de maca y cómo estas determinan la formación de bencilamina, un precursor directo de la formación de las amidas bioactivas, además de evaluar vías colaterales que resultan en la formación de productos no deseables, como ácido benzoico. El proyecto requirió poder emular el secado en campo bajo condiciones de laboratorio en periodos cortos de tiempo, y no 10 semanas como ocurre en el secado tradicional. Se llevó a cabo un monitoreo de los metabolitos que participan en la formación de bencilamina y de los productos terminales del proceso de secado. Para el monitoreo de los metabolitos, se utilizaron tres métodos de extracción por ultrasonido en diferentes solventes: 70% metanol, diclorometano y diclorometano acidificado y se analizaron los extractos por cromatografía líquida o de gases.Tesi

Research progress in the anti-cancer activity and related mechanisms of arenobufagin

Toad venom is an active extract of toad, which is processed by distilling or drying at high temperature the venom secreted from the skin glands and ear-side glands of Toad Chinensis. As a natural product that has been used to treat diseases in China for thousands of years, toad venom has many pharmacological effects such as heart strengthening, analgesia, anti-myocardial ischemia, anti-endotoxin shock, and anti-cancer. Arenobufagin (ARE) is one of the main chemical components of toad venom, and its anti-cancer mechanism has been increasingly clarified in the past decade. ARE can play an anti-cancer role through a variety of ways, such as inducing apoptosis and/or autophagy of cancer cells, necrosis, and cell cycle arrest, inhibiting cancer cell migration and invasion, and inhibiting angiogenesis. The current research on ARE mainly focuses on the selective toxicity of cancer cells and the molecular mechanism of anti-cancer, mostly at the cellular and animal levels. Due to the large toxic and side effects of ARE, unclear targets and unclear pharmacokinetic characteristics, ARE has not yet entered the clinical application in Western medicine. This article summarizes relevant research results on the anti-cancer activity and molecular mechanism of ARE, and its combination with other anti-cancer drugs in order to provide a new direction for improving the anti-cancer mechanism of ARE