Hyperoside protects human primary melanocytes against H2O2-induced oxidative damage

Abstract

Cuscutae semen has been shown to have beneficial effects in the treatment of vitiligo, recorded in the Chinese Pharmacopoeia, whereas the effects of its constituent compounds remains to be elucidated. Using a tetrazolium bromide assay, the present study found that hyperoside (0.5–200 µg/ml) significantly increased the viability of human melanocytes in a time- and dose-dependent manner. The present study used a cell model of hydrogen peroxide (H2O2)-induced oxidative damage to examine the effect of hyperoside on human primary melanocytes. The results demonstrated that hyperoside pretreatment for 2 h decreased cell apoptosis from 54.03±9.11 to 17.46±3.10% in the H2O2-injured melanocytes. The levels of oxidative stress in the mitochondrial membrane potential of the melanocytes increased following hyperoside pretreatment. The mRNA and protein levels of B-cell lymphoma-2/Bcl-2-associated X protein and caspase 3 were regulated by hyperoside, and phosphoinositide 3-kinase/AKT and mitogen-activated protein kinase signaling were also mediated by hyperoside. In conclusion, the results of the present study demonstrated that hyperoside protected the human primary melanocytes against oxidative damage.

Safety and efficacy of hydrogen peroxide topical solution, 40% (w/w), in patients with seborrheic keratoses: Results from 2 identical, randomized, double-blind, placebo-controlled, phase 3 studies (A-101-SEBK-301/302)

“…[11][12][13][14] It is considered that with penetration of the proprietary HP40 solution into the SK lesion, HP may act not only through its direct oxidation of organic tissues, generation of reactive oxygen species, and local lipid peroxidation but also through generation of local concentrations of oxygen that are toxic to SK cells. [15][16][17][18] Recent ex vivo skin implant studies of neonatal foreskin suggest that HP40 leads to less cytotoxicity and greater melanocyte viability than with liquid nitrogen. 19 The number of treatment sessions for each lesion in these studies was limited by protocol design to 2, and the optimal number of treatment sessions to clear all lesions was not evaluated.…”

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

“…Park et al [15] found that HYP is an effective compound to protect cells against oxidative stress via haem oxygenase-1 (HO-1) induction. Yang et al [16] revealed that HYP protected the human primary melanocytes against oxidative damage through phosphoinositide 3kinase/AKT signally pathways .…”

Geniposide prevents H2 O2 -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

“…Activation of the PI3K–Akt signalling pathway protects against oxidative stress‐induced cell death . Specifically, geniposide protects cells from H 2 O 2 ‐induced apoptosis by activating the PI3K–Akt signalling pathway .…”

“…Specifically, geniposide protects cells from H 2 O 2 ‐induced apoptosis by activating the PI3K–Akt signalling pathway . The Bcl‐2 and caspase families, which are crucial proteins involved in the apoptosis response induced by oxidative stress, are downstream molecules of the PI3K–Akt signalling pathway. Pre‐treatment of H 2 O 2 ‐induced melanocytes with geniposide increased expression of the anti‐apoptotic protein Bcl‐2 and decreased expression of Bax, a pro‐apoptotic protein belonging to the Bcl‐2 family.…”