Pharmacological and Non-Pharmacological Agents versus Bovine Colostrum Supplementation for the Management of Bone Health Using an Osteoporosis-Induced Rat Model

Osteoporosis is defined by loss of bone mass and deteriorated bone microarchitecture. The present study compared the effects of available pharmacological and non-pharmacological agents for osteoporosis [alendronate (ALE) and concomitant supplementation of vitamin D (VD) and calcium (Ca)] with the effects of bovine colostrum (BC) supplementation in ovariectomized (OVX) and orchidectomized (ORX) rats. Seven-month-old rats were randomly allocated to: (1) placebo-control, (2) ALE group (7.5 μg/kg of body weight/day/5 times per week), (3) VD/Ca group (VD: 35 μg/kg of body weight/day/5 times per week; Ca: 13 mg/kg of body weight/day/3 times per week), and (4) BC supplementation (OVX: 1.5 g/day/5 times per week; ORX: 2 g/day/5 times per week). Following four months of supplementation, bone microarchitecture, strength and bone markers were evaluated. ALE group demonstrated significantly higher Ct.OV, Ct.BMC, Tb.Th, Tb.OV and Tb.BMC and significantly lower Ct.Pr, Tb.Pr, Tb.Sp, Ct.BMD and Tb.BMD, compared to placebo (p < 0.05). BC presented significantly higher Ct.Pr, Ct.BMD, Tb.Pr, Tb.Sp, and Tb.BMD and significantly lower Ct.OV, Ct.BMC, Tb.Th, Tb.OV and Tb.BMC compared to ALE in OVX rats (p < 0.05). OVX rats receiving BC experienced a significant increase in serum ALP and OC levels post-supplementation (p < 0.05). BC supplementation may induce positive effects on bone metabolism by stimulating bone formation, but appear not to be as effective as ALE

Photography-based taxonomy is inadequate, unnecessary, and potentially harmful for biological sciences

The question whether taxonomic descriptions naming new animal species without type specimen(s) deposited in collections should be accepted for publication by scientific journals and allowed by the Code has already been discussed in Zootaxa (Dubois & Nemésio 2007; Donegan 2008, 2009; Nemésio 2009a–b; Dubois 2009; Gentile & Snell 2009; Minelli 2009; Cianferoni & Bartolozzi 2016; Amorim et al. 2016). This question was again raised in a letter supported by 35 signatories published in the journal Nature (Pape et al. 2016) on 15 September 2016. On 25 September 2016, the following rebuttal (strictly limited to 300 words as per the editorial rules of Nature) was submitted to Nature, which on 18 October 2016 refused to publish it. As we think this problem is a very important one for zoological taxonomy, this text is published here exactly as submitted to Nature, followed by the list of the 493 taxonomists and collection-based researchers who signed it in the short time span from 20 September to 6 October 2016

Un calostro bovino neuroprotector atenúa la apoptosis inducida por dexametasona en células osteoblásticas MC3T3-E1

Este estudio ha sido financiado por la Unión Europea mediante una MSCA-RISE-Marie Skłodowska-Curie Research and Innovation Staff Exchange (RISE) (Grant agreement ID: 778277). El proyecto, en toda su extensión, ha pretendido crear una colaboración intersectorial (instituciones académicas e industriales) para intercambiar conocimientos y experiencias con la finalidad de crear un producto nutracéutico innovador, basado en el calostro, para prevenir la osteoporosis. La osteoporosis constituye un importante problema de salud pública. Se prevé un aumento importante de la carga económica de las fracturas osteoporóticas en la Unión Europea hasta 2025. Estas estimaciones pueden indicar una ineficacia de los tratamientos farmacológicos actuales para la osteoporosis. Por tanto, se necesitan agentes innovadores para reducir la carga de la osteoporosis. El calostro es un agente prometedor frente a la pérdida de masa ósea ya que contiene componentes que intervienen directamente en el metabolismo óseo. Sin embargo, la posibilidad de su uso como agente nutracéutico para la osteoporosis sólo ha recibido atención dentro de la comunidad científica. Los conocimientos sobre los efectos del calostro en el metabolismo óseo aún no se han trasladado al mercado y, la industria, aunque posee los conocimientos para el desarrollo de productos, carece de experiencia en investigación. En definitiva, lo que dificulta la creación de un producto innovador basado en el calostro para la prevención de la osteoporosis es la ausencia de una colaboración intersectorial. Concretamente, la osteoporosis inducida por glucocorticoides (OIG) es una de las formas secundarias más frecuentes de osteoporosis. La OIG se debe en parte al proceso de apoptosis que experimentan los osteoblastos y osteocitos. Para el presente estudio se desarrolló un modelo celular de apoptosis exponiendo a una línea celular osteoblástica, MC3T3-E1, al glucorticoide dexametasona (DEX) en un rango de concentraciones en el medio de cultivo desde 0 hasta 700 μM. El daño inducido por la DEX se estudió en presencia y ausencia de tratamiento con un calostro bovino (0,1-5,0 mg/mL) con el fin de conocer la posible protección que puede ejercer frente a la apoptosis celular inducida por el glucocorticoide. El calostro evitó la disminución de la viabilidad celular y el aumento de la activación de la caspasa-3 y del estrés oxidativo causados por la exposición a DEX. Las células, tras el tratamiento con calostro junto con DEX, mostraron niveles más altos de p-ERK1/2 y niveles más bajos de Bcl-XL, Bax y Hsp70. Nuestros datos apoyan la noción de que el calostro puede ser capaz de reducir la apoptosis inducida por DEX posiblemente a través de la activación de la vía ERK y la modulación del sistema Hsp70. Proporcionamos pruebas preliminares de cómo el calostro bovino, como producto lácteo complejo y multicomponente, además de su acción neuroprotectora, puede afectar a la supervivencia de las células osteoblásticas sometidas a apoptosis. Estos resultados prueban que este calostro posee capacidad reductora de la apoptosis inducida por DEX, posiblemente a través de la activación de la vía ERK y la modulación del sistema Hsp70.Glucocorticoid-induced osteoporosis (GIO) is one of the most common secondary forms of osteoporosis. GIO is partially due to the apoptosis of osteoblasts and osteocytes. In addition, high doses of dexamethasone (DEX), a synthetic glucocorticoid receptor agonist, induces neurodegeneration by initiating inflammatory processes leading to neural apoptosis. Here, a neuroprotective bovine colostrum against glucocorticoid-induced neuronal damage was investigated for its anti-apoptotic activity in glucocorticoid-treated MC3T3-E1 osteoblastic cells. A model of apoptotic osteoblastic cells was developed by exposing MC3T3-E1 cells to DEX (0–700 μM). Colostrum co-treated with DEX was executed at 0.1–5.0 mg/mL. Cell viability was measured for all treatment schedules. Caspase-3 activation was assessed to determine both osteoblast apoptosis under DEX exposure and its potential prevention by colostrum co-treatment. Glutathione reduced (GSH) was measured to determine whether DEX-mediated oxidative stress-driven apoptosis is alleviated by colostrum co-treatment. Western blot was performed to determine the levels of p-ERK1/2, Bcl-XL, Bax, and Hsp70 proteins upon DEX or DEX plus colostrum exposure. Colostrum prevented the decrease in cell viability and the increase in caspase-3 activation and oxidative stress caused by DEX exposure. Cells, upon colostrum co-treated with DEX, exhibited higher levels of p-ERK1/2 and lower levels of Bcl-XL, Bax, and Hsp70. Our data support the notion that colostrum may be able to reduce DEX-induced apoptosis possibly via the activation of the ERK pathway and modulation of the Hsp70 system. We provided preliminary evidence on how bovine colostrum, as a complex and multi-component dairy product, in addition to its neuroprotective action, may affect osteoblastic cell survival undergoing apoptosis.MSCA-RISE-Marie Skłodowska-Curie Research and Innovation Staff Exchange (RISE) grant funded by the European UnionDepto. de Farmacología, Farmacognosia y BotánicaFac. de FarmaciaTRUEpu