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Hyperoside protects human osteoblasts from phthalate-induced mitochondrial dysfunction, oxidative stress, and
Ekramy M Elmorsy1, Huda A Al Doghaither2, Ayat B Al-Ghafari3
1Center for Health Research, Northern Border University, Arar 91431, Saudi Arabia.
Toxicology and Applied Pharmacology
|August 7, 2025
Summary
Hyperoside (HYP) protects human osteoblasts from butyl cyclohexyl phthalate (BCP) bone toxicity. HYP enhances mitochondrial function and reduces oxidative stress and apoptosis, offering a potential therapeutic for environmental bone damage.
Area of Science:
- Environmental Toxicology
- Cell Biology
- Biochemistry
Background:
- Butyl cyclohexyl phthalate (BCP) is an environmental contaminant that induces osteoblast dysfunction.
- BCP toxicity involves oxidative stress, mitochondrial damage, and apoptosis, impacting bone health.
- Flavonoids, like hyperoside (HYP), are investigated for their protective properties against environmental toxins.
Purpose of the Study:
- To investigate the protective effects of hyperoside (HYP) against BCP-induced toxicity in human osteoblasts.
- To elucidate the molecular mechanisms underlying BCP's osteotoxicity and HYP's protective actions.
- To evaluate HYP's potential as a therapeutic agent against environmental bone toxicity.
Main Methods:
- Molecular docking was used to predict binding interactions of BCP and HYP with target proteins.
- In vitro assays assessed BCP's cytotoxicity, mitochondrial function (ATP, membrane potential, complex activities), mitophagy (PINK1/PARKIN), oxidative stress (biomarkers), and apoptosis (caspases, Bax/Bcl2).
- The effects of HYP co-treatment on these BCP-induced changes were evaluated, including Nrf2/HO-1 pathway activation.
Main Results:
- BCP exhibited dose-dependent cytotoxicity, impairing mitochondrial function, suppressing mitophagy, increasing oxidative stress, and activating apoptosis in osteoblasts.
- Molecular docking indicated strong binding of BCP and HYP to proteins involved in oxidative stress and apoptosis.
- HYP co-treatment reversed BCP's toxic effects, restoring osteoblast viability, secretory function, and mitophagy.
- HYP mitigated oxidative stress via Nrf2/HO-1 activation and prevented apoptosis by inhibiting caspases and normalizing the Bax/Bcl2 ratio.
Conclusions:
- Hyperoside (HYP) demonstrates significant cytoprotective effects against butyl cyclohexyl phthalate (BCP)-induced osteoblast toxicity.
- HYP acts by enhancing mitochondrial quality control, activating the Nrf2/HO-1 antioxidant pathway, and inhibiting apoptosis.
- This study highlights HYP as a promising therapeutic candidate for managing environmental bone toxicity, targeting key pathways like mitophagy and redox balance.
