Journal
ANTIOXIDANTS
Volume 10, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/antiox10081209
Keywords
ferulic acid; total body irradiation; bone marrow microenvironment; stem cell senescence; bone marrow injury; reactive oxygen species; antioxidant defense system
Funding
- National Research Foundation (NRF) - Ministry of Science, Information and Communications Technology and Future Planning [2018R1D1A1B07046563, 2020R1C1C1004968, 2021R1A2C2006032, 2021R111A1A01044453]
- RDA, Ministry of Agriculture and Forestry, Republic of Korea [PJ013394022021]
- National Research Foundation of Korea [2018R1D1A1B07046563, 2020R1C1C1004968, 2021R1A2C2006032] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- Rural Development Administration (RDA), Republic of Korea [PJ013394022021] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Ferulic acid, as a dietary antioxidant, can protect against systemic damages caused by TBI by restoring disorders in bone formation, osteoclast activation, and adipocyte activation, thereby preventing stem cell senescence and bone mass loss.
While total body irradiation (TBI) is an everlasting curative therapy, the irradiation can cause long-term bone marrow (BM) injuries, along with senescence of hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs) via reactive oxygen species (ROS)-induced oxidative damages. Thus, ameliorating or preventing ROS accumulation and oxidative stress is necessary for TBI-requiring clinical treatments. Here, we explored whether administration of ferulic acid, a dietary antioxidant, protects against TBI-mediated systemic damages, and examined the possible mechanisms therein. Sublethal TBI (5 Gy) decreased body growth, lifespan, and production of circulating blood cells in mice, together with ROS accumulation, and senescence induction of BM-conserved HSCs and MSCs. TBI also impaired BM microenvironment and bone mass accrual, which was accompanied by downregulated osteogenesis and by osteoclastogenic and adipogenic activation in BM. Long-term intraperitoneal injection of ferulic acid (50 mg/kg body weight, once per day for 37 consecutive days) protected mice from TBI-mediated mortality, stem cell senescence, and bone mass loss by restoring TBI-stimulated disorders in osteogenic, osteoclastic, and adipogenic activation in BM. In vitro experiments using BM stromal cells supported radioprotective effects of ferulic acid on TBI-mediated defects in proliferation and osteogenic differentiation. Overall, treatment with ferulic acid prevented TBI-mediated liver damage and enhanced endogenous antioxidant defense systems in the liver and BM. Collectively, these results support an efficient protection of TBI-mediated systemic defects by supplemental ferulic acid, indicating its clinical usefulness for TBI-required patients.
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