We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Anthocyanin-rich polyphenols from Hibiscus syriacus activate autophagy to reverse polystyrene microplastic-induced osteogenic dysfunction
AI summary Read the abstract
Researchers found that anthocyanin-rich polyphenols from Hibiscus syriacus can restore bone cell function impaired by polystyrene microplastic exposure in both cell culture and zebrafish models. The study suggests that these plant compounds activate autophagy pathways to reverse microplastic-induced cellular aging and osteogenic dysfunction, indicating potential protective effects of dietary polyphenols against microplastic-related skeletal impacts.
BACKGROUND: The environmental accumulation of microplastics (MPs), defined as plastic particles ≤5 mm, has emerged as a critical global health concern, particularly owing to their potential to impair skeletal development and bone homeostasis. PURPOSE: This study aimed to determine whether anthocyanin-rich polyphenols extracted from Hibiscus syriacus L. (AH) could restore osteogenesis impaired by polystyrene MPs (PS-MPs) by targeting osteoblast senescence and autophagy regulation. METHODS: MC3T3-E1 preosteoblasts were exposed to PS-MPs followed by treatment with AH, and osteogenic recovery was evaluated via alkaline phosphatase (ALP) activity, calcium mineralization, and expression of osteogenic markers (RUNX2, SP7, and ALP) over 14 days. Senescence-associated secretory phenotype (SASP) markers (Tnf, Mmp13, Il6, and Il1b), key senescence regulators (p21, p27, MMP13, and Lamin B1), and autophagy markers (p62 and LC3B) were assessed using RT-qPCR, western blotting, and immunofluorescence. Zebrafish larvae were employed as an in vivo model to evaluate vertebral mineralization using calcein staining, as well as the expression of SASP osteogenic genes. RESULTS: PS-MP exposure markedly reduced ALP activity, mineral deposition, and osteogenic gene/protein expression, while elevating senescence markers, indicative of severe osteoblast dysfunction. AH treatment significantly reversed these effects, effectively restoring ALP activity and mineralization. Furthermore, AH activated autophagy, as evidenced by increased LC3B and reduced p62 expression. In zebrafish, AH ameliorated PS-MP-induced defects in vertebral mineralization, reduced skeletal malformations, and upregulated osteogenic genes. CONCLUSION: AH mitigates PS-MP-induced osteogenic dysfunction through the dual modulation of osteoblast senescence and autophagy activation, supporting its potential as a natural therapeutic strategy against MP-related skeletal disorders.
More Papers Like This
Human osteoblast-like cells exhibit anabolic attenuation and catabolic phenotypic signals after exposure to polystyrene microplastics
AI summary Read the abstract
Researchers exposed human bone-building cells (osteoblast-like cells) to polystyrene microplastics in a lab setting. The cells showed reduced signals linked to building new bone and increased signals linked to bone breakdown, suggesting microplastics may affect cell activity related to bone health.
Effects of Polystyrene Microplastics on Bone-related Protein Expression, Mineralization Capacity, and Mitochondrial Function in Osteoblast-like Cells (mg-63)
AI summary Read the abstract
Osteoblast-like cells (MG-63) were exposed to polystyrene microplastics at 5–50 µg/mL, and bone-related protein expression, mineralisation capacity, and mitochondrial function were assessed. PS-MPs were internalised and reduced mineralisation and osteocalcin levels while impairing mitochondrial bioenergetics, suggesting microplastics may negatively affect bone cell function.
Tagetes erecta L. polyphenols restore osteogenesis impaired by polystyrene microplastics via NRF2-mediated ER–mitochondrial homeostasis
AI summary Read the abstract
Scientists found that tiny plastic particles called microplastics can weaken bone formation by causing cell stress and damage in bone-building cells—at least in lab cells and zebrafish. The good news: a plant extract from marigold flowers (Tagetes erecta) was able to reverse this damage by boosting the cells' natural antioxidant defenses. While this is early-stage research in animals and cells (not yet tested in humans), it suggests marigold-derived compounds could one day help protect bone health as microplastic pollution continues to rise.
Polystyrene microplastics disrupt osteogenic differentiation via lysosome-mediated mitochondrial dysfunction: Protective role of mTOR signaling
AI summary Read the abstract
Researchers identified a mechanistic pathway by which polystyrene microplastics impair bone formation in zebrafish and mouse preosteoblasts: PS-MPs accumulate in lysosomes, trigger mitochondrial dysfunction, and suppress osteogenic differentiation. Activation of the mTOR signaling pathway was found to partially protect against this bone toxicity.
Polystyrene microplastics induces senescence of osteocytes by activating the cyclooxygenase-2 signaling pathway
AI summary Read the abstract
Researchers found that polystyrene microplastics can be taken up by osteocytes, the most abundant cells in bone tissue, and cause them to undergo premature aging through a process called senescence. The microplastics triggered oxidative stress and activated a specific inflammatory signaling pathway involving cyclooxygenase-2. The study suggests that microplastic exposure could potentially impair bone health by disrupting the normal function of the cells responsible for maintaining bone tissue.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.