A Neuroprotective Bovine Colostrum Attenuates Apoptosis in Dexamethasone-Treated MC3T3-E1 Osteoblastic Cells

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

Seasonal variation in the nutrient profile of Arthrospira fusiformis biomass harvested from an Ethiopian soda lake, Lake Chitu

The extent of seasonal variation in the nutrient profile of Arthrospira biomass harvested from Lake Chitu was investigated to evaluate the variability of the quality of the product over a period of a year. Protein content varied from 47.9 to 55.7% for wet season biomass samples and from 39.2 to 40.8% for dry season samples. Dry season samples were characterized by relatively higher carbohydrate values (38.0–41.3%). Higher proportion of amino acids and unsaturated fatty acids were recorded for biomass harvested in wet season. Similarly, higher contents of phytonutrients (pigments) were recorded for wet season biomass samples: chlorophyll a (8.2–10.3 mg g−1), phycobiliproteins (104.1–120.7 mg g−1), total carotenoids (3.17–4.31 mg g−1), and β-carotene (1.24–1.61 mg g−1). The contents of Na and K were higher for a dry season biomass whereas other major (Ca, P, Mg) and trace (Mn, Fe, Cu, Zn, Se) minerals were found relatively in higher quantities in a wet season biomass. The nutritional composition of Arthrospira from Lake Chitu was found to be relatively comparable to that found in commercial Arthrospira products in the market. The significance of the findings is discussed in relation to potential sustainable production of Arthrospira biomass from this lake

Acción anti-apoptótica de un calostro bovino en un modelo celular de osteoporosis

La osteoporosis inducida por glucocorticoides es una de las formas secundarias más comunes de osteoporosis, debida en parte a la apoptosis de osteoblastos y osteocitos. En el presente trabajo, se han investigado los efectos de un calostro bovino en un modelo celular de osteoporosis obtenido a partir de la exposición de células osteoblásticas MC3T3-E1 a la DEX, en un rango de concentración (0-700 μM). El co-tratamiento de las células con el calostro bovino se realizó a una concentración de 0,1-5,0 mg/mL. Se determinó la activación de la caspasa-3 para evaluar el grado de apoptosis de los osteoblastos bajo la exposición a DEX y su posible prevención mediante el co-tratamiento con calostro. Se midieron los niveles de glutation reducido (GSH) para determinar si la apoptosis mediada por el estrés oxidativo de la DEX se veía disminuida por el co-tratamiento con calostro. Finalmente, mediante Western blot, se determinaron los niveles de las proteínas p-ERK1/2, Bcl-XL, Bax y Hsp70 tras la exposición a DEX o DEX más calostro. El calostro evitó la disminución de la viabilidad celular y el aumento de la activación de la caspasa-3 y el estrés oxidativo, causados por la exposición a la DEX. Las células sometidas a un tratamiento conjunto de calostro y DEX mostraron mayores niveles de p-ERK1/2 y menores niveles de Bcl-XL, Bax y Hsp70. Estos resultados prueban que el calostro posee capacidad de reducir la apoptosis inducida por DEX posiblemente a través de la activación de la vía ERK y la modulación del sistema Hsp70

A neuroprotective bovine colostrum attenuates apoptosis in dexamethasone‐treated mc3t3‐e1 osteoblastic cells

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. © 2021 by the authors