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Published on: August 13, 2019
Hyperoside Modulates the Estrogen-PI3K/VEGF Axis to Ameliorate Oxidative Damage-Induced Inhibition of Bone Formation
Shuo Wang1, Wei Feng2, Xueqin Feng1
1Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, China.
Objective:
This study aims to investigate how hyperoside (HYP) alleviates oxidative stress-induced osteoporosis, its molecular mechanisms, and its impact on osteoblast differentiation, oxidative damage, and the estrogen-PI3K/VEGF signaling pathway.
Methods:
The osteoblast differentiation model was induced using dexamethasone, and osteoblast-related markers like ALP, NO, GSH, MDA, and SOD were measured post-HYP intervention. A zebrafish model was used to assess HYP's impact on ROS and bone formation. Network pharmacology identified key oxidative stress and osteoporosis targets, with HYP's binding affinity confirmed via molecular docking and simulation. RT-qPCR verified the expression of key pathway targets.
Results:
HYP can counteract dexamethasone-induced inhibition of osteoblast differentiation, boost ALP, NO, GSH, and SOD levels, and lower MDA levels in osteoblasts. It also reduces ROS accumulation and enhances bone formation in zebrafish. Network pharmacology identified a common oxidative stress and osteoporosis target, with molecular docking confirming HYP's stable binding. RT-qPCR showed HYP significantly upregulates SRC, PI3K, AKT1, and e-NOS, activating the estrogen-PI3K/VEGF pathway.
Conclusion:
HYP plays an anti-oxidative stress effect through targeted regulation of estrogen-PI3K/VEGF signal axis, and then promotes osteoblast differentiation and bone formation, which provides a new potential candidate drug and experimental basis for the treatment of osteoporosis.
Insights
Hyperoside (HYP) combats oxidative stress and promotes osteoblast differentiation, offering a potential new treatment for osteoporosis by activating the estrogen-PI3K/VEGF pathway.
Area of Science:
- Biochemistry
- Molecular Biology
- Pharmacology
Background:
- Osteoporosis is a growing concern linked to oxidative stress.
- Understanding the molecular mechanisms of potential therapeutic agents is crucial.
Purpose of the Study:
- To investigate hyperoside's (HYP) efficacy in alleviating oxidative stress-induced osteoporosis.
- To elucidate HYP's impact on osteoblast differentiation and the estrogen-PI3K/VEGF signaling pathway.
Main Methods:
- Osteoblast differentiation induced by dexamethasone; measured markers (ALP, NO, GSH, MDA, SOD).
- Zebrafish model used to assess reactive oxygen species (ROS) and bone formation.
- Network pharmacology, molecular docking, and RT-qPCR utilized to identify targets and verify pathways.
Main Results:
- HYP counteracted dexamethasone-induced inhibition, improving osteoblast markers and reducing oxidative damage.
- HYP reduced ROS and enhanced bone formation in zebrafish.
- RT-qPCR confirmed HYP upregulates SRC, PI3K, AKT1, and e-NOS, activating the estrogen-PI3K/VEGF pathway.
Conclusions:
- Hyperoside exerts anti-oxidative effects by regulating the estrogen-PI3K/VEGF pathway.
- HYP promotes osteoblast differentiation and bone formation.
- HYP presents a potential therapeutic candidate for osteoporosis treatment.
