Protective effect of hyperoside against hydrogen peroxide-induced dysfunction and oxidative stress in osteoblastic MC3T3-E1 cells

Abstract

Oxidative stress can induce apoptosis and decrease activities of osteoblasts. Hyperoside (HYP) is a potent antioxidant derived from Chinese herb. This study aims to evaluate the protective effects provided by HYP to osteoblastic MC3T3-E1 cells. MC3T3-E1 cells were pre-treated with HYP for 24 h before being treated with 0.3 mM hydrogen peroxide (H 2 O 2) for 24 h. Cell viability, flow cytometric analysis and mRNA expression of alkaline phosphatase (ALP), collagen I (COL-I) and osteocalcin (OCN) in MC3T3-E1 cells were examined. We next examined apoptosis-related and mitogen-activated protein kinase (MAPK) related proteins in HYP and H 2 O 2 groups. HYP over the dose of 40 lmol/L could obviously increase the MC3T3-E1 cell viability at 24 h and 48 h (p < .05). HYP significantly (p < .05) increased mRNA expression of ALP, COL-I and OCN than H 2 O 2 group. Moreover, HYP decreased the apoptosis rate and apoptosis-related proteins that induced by H 2 O 2. In addition, HYP decreased the production of phosphorylated Jun N-terminal kinase (JNK) and p38 levels of osteoblastic MC3T3-E1 cells induced by H 2 O 2. These results demonstrated that the protective effect provided by HYP to osteoblastic MC3T3-E1 cells was mediated, at least in part, via inhibition of MAPK signalling pathway and oxidative damage of the cells.

Protective Effects and Mechanism of Hyperoside in PC12 Cells Against Oxidative Stress Injury Induced by Hydrogen Peroxide

“…It has been reported to alleviate the effects of oxidative stress damage, to varying degrees, in the treatment of inflammatory apoptosis. 12,13 H 2 O 2 acts as an inducer of oxidative stress in vitro and can induce apoptosis in many different cell types, but H 2 O 2 can be inhibited by antioxidants. 14 Therefore, this study explored the role of hyperoside as an antioxidant and studied its protective mechanism in H 2 O 2 -treated PC12 cells.…”

“…11 It has also been shown that hyperoside can reduce H 2 O 2 -induced osteoblast MC3T3-E1 phosphorylation Jun terminal kinase (JNK) and lower P38 levels by inhibiting mitogen-activated protein kinase (MAPK) signaling; it reduces H 2 O 2 -induced cell apoptosis and apoptosis-related proteins. 12 However, there are only a few studies that have explored the protective mechanism of hyperoside in alleviating the oxidative stress injury of neurons. In this study, PC12 rat pheochromocytoma cells, a sympathetic nervous system tumor-cell line widely used to study neuronal injury-related models and highly similar to dopaminergic neurons in structure and function, were selected to establish an H 2 O 2 -induced oxidative-injury model.…”

Hyperoside Suppresses Osteoclasts Differentiation and Function through Down-Regulating TRAF6/p38 MAPK Signaling Pathway

“…In recent years, HP has also been studied in anti-osteoporosis. HP can protect MC3T3-E1 from oxidative stress via inhibiting the MAPK signaling pathway and oxidative damage of the cells [20], reduce the apoptosis and autophagy rate of MC3T3-E1. In addition, HP also has a good anti-osteoporosis performance in OVX mice through NF-κB signaling pathway.…”

Osteoprotective Effects of ‘Anti-Diabetic’ Polyherbal Mixture in Type 1 Diabetic Rats

“…Supplementation with quercetin and arbutin ameliorates bone loss by reducing bone resorption [25,31,32,[66][67][68] through the suppression of osteoclasts activity and the stimulation of osteoblast activity [69][70][71][72][73]. Hyperoside protects osteoblasts from oxidative stress [74,75], while astragalin stimulates differentiation of osteoblasts [76]. Additionally, quinic acid promotes osteoblasts differentiation through activation of the Wnt/β-catenin pathway, while caftaric acid modulates RunX2 and RANKL/OPG signalling pathways [77].…”