ArticleOxidative medicine and cellular longevity2020
Proanthocyanidins-Mediated Nrf2 Activation Ameliorates Glucocorticoid-Induced Oxidative Stress and Mitochondrial Dysfunction in Osteoblasts.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Linking the relationship between drug-induced osteoporosis and the gut microbiota.Frontiers in endocrinology · 2026Review
- Mitigating mitochondrial dysfunction: a novel strategy for Chinese botanical drugs against osteoporosis.Frontiers in pharmacology · 2026Review
- Shugan Xiaozhi Decoction attenuates nonalcoholic steatohepatitis by modulating oxidative stress and AMPK pathway.BMC complementary medicine and therapies · 2025Article
- Curcumin preserves bone health compromised by diabetes by inhibiting osteoporosis through regulation of the SIRT3/FoxO3a signalling pathway.Scientific reports · 2025Article
- Therapeutic Potential of Proanthocyanidins in Dentistry: A Focus on Periodontal Disease and on Dental Implants in Osteoporotic Patients.Antioxidants (Basel, Switzerland) · 2025Review
- Nrf2 Activation as a Therapeutic Target for Flavonoids in Aging-Related Osteoporosis.Nutrients · 2025Review
- The biological functions of proanthocyanidin and its application in pig production.Frontiers in veterinary science · 2025Review
- Recent advances in layer-by-layer assembly scaffolds for co-delivery of bioactive molecules for bone regeneration: an updated review.Journal of translational medicine · 2024Review
- Grape seed extract prevents oestrogen deficiency-induced bone loss by modulating the gut microbiota and metabolites.Microbial biotechnology · 2024Article
- Mitochondrial Dysfunction in Periodontitis and Associated Systemic Diseases: Implications for Pathomechanisms and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- The Therapeutic Potential of Two Egyptian Plant Extracts for Mitigating Dexamethasone-Induced Osteoporosis in Rats: Nrf2/HO-1 and RANK/RANKL/OPG Signals.Antioxidants (Basel, Switzerland) · 2024Article
- Apocynin exerts cytoprotective effects on dexamethasone-induced osteoblasts by inhibiting oxidative stress through the Nrf2 signalling pathway.Journal of cellular and molecular medicine · 2023Article
- Glucocorticoid-induced activation of NOX/ROS/NF-κB signaling in MSCs contributes to the development of GONFH.Apoptosis : an international journal on programmed cell death · 2023Article
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- Targeted activation of Nrf2/HO-1 pathway by Corynoline alleviates osteoporosis development.Food science & nutrition · 2023Article
- Identification of kukoamine a as an anti-osteoporosis drug target using network pharmacology and experiment verification.Molecular medicine (Cambridge, Mass.) · 2023Article
- Bioactivity, Molecular Mechanism, and Targeted Delivery of Flavonoids for Bone Loss.Nutrients · 2023Review
- Oxidative Stress and Natural Antioxidants in Osteoporosis: Novel Preventive and Therapeutic Approaches.Antioxidants (Basel, Switzerland) · 2023Review
- Exosomes from Adipose-Derived Stem Cells Alleviate Dexamethasone-Induced Bone Loss by Regulating the Nrf2/HO-1 Axis.Oxidative medicine and cellular longevity · 2023Article
- Exogenous Hydrogen Sulfide Mitigates Oxidative Stress and Mitochondrial Damages Induced by Polystyrene Microplastics in Osteoblastic Cells of Mice.Disease markers · 2023Article
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10 authors at 1 institution in 1 country.
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Abstract
The widespread use of therapeutic glucocorticoids has increased the frequency of glucocorticoid-induced osteoporosis (GIOP). One of the potential pathological processes of GIOP is an increased level of oxidative stress and mitochondrial dysfunction, which eventually leads to osteoblast apoptosis. Proanthocyanidins (PAC) are plant-derived antioxidants that have therapeutic potential against GIOP. In our study, a low dose of PAC was nontoxic to healthy osteoblasts and restored osteogenic function in dexamethasone- (Dex-) treated osteoblasts by suppressing oxidative stress, mitochondrial dysfunction, and apoptosis. Mechanistically, PAC neutralized Dex-induced damage in the osteoblasts by activating the Nrf2 pathway, since silencing Nrf2 partly eliminated the protective effects of PAC. Furthermore, PAC injection restored bone mass and promoted the expression of Nrf2 in the distal femur of Dex-treated osteoporotic rats. In summary, PAC protect osteoblasts against Dex-induced oxidative stress and mitochondrial dysfunction via the Nrf2 pathway activation and may be a promising drug for treating GIOP.
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