دورية أكاديمية
A neuroprotective bovine colostrum attenuates apoptosis in dexamethasone‐treated mc3t3‐e1 osteoblastic cells
| العنوان: | A neuroprotective bovine colostrum attenuates apoptosis in dexamethasone‐treated mc3t3‐e1 osteoblastic cells |
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| المؤلفون: | Martin‐aragon S., Bermejo‐bescós P., Benedí J., Raposo C., Marques F., Kydonaki E.K., Gkiata P., Koutedakis Y., Ntina G., Carrillo A.E., Amorim T. |
| المصدر: | International Journal of Molecular Sciences ; https://www.scopus.com/inward/record.uri?eid=2-s2.0-85115349424&doi=10.3390%2fijms221910195&partnerID=40&md5=ed21b6f796e6c0ad7730827d913ed057Test |
| سنة النشر: | 2021 |
| المجموعة: | University of Thessaly Institutional Repository / Ιδρυματικό Αποθετήριο Πανεπιστημίου Θεσσαλίας |
| مصطلحات موضوعية: | caspase 3, dexamethasone, glutathione, heat shock protein 70, mitogen activated protein kinase 1, mitogen activated protein kinase 3, protein Bax, protein bcl xl, reactive oxygen metabolite, glucocorticoid, neuroprotective agent, animal cell, antiapoptotic activity, apoptosis, Article, bovine, cell survival, cell viability, colostrum, controlled study, dairy product, enzyme activation, human, human cell, MAPK signaling, MC3T3-E1 cell line, nerve cell lesion, neuroprotection, neurotoxicity, nonhuman |
| الوصف: | 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. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 16616596 |
| العلاقة: | http://hdl.handle.net/11615/76396Test |
| DOI: | 10.3390/ijms221910195 |
| الإتاحة: | https://doi.org/10.3390/ijms221910195Test http://hdl.handle.net/11615/76396Test |
| رقم الانضمام: | edsbas.2CB45DBE |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 16616596 |
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| DOI: | 10.3390/ijms221910195 |