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Source: J Cell Mol Med
Condition: Vitiligo

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Total 2 results found since Jan 2013.

HMGB1 deficiency reduces H2 O2 -induced oxidative damage in human melanocytes via the Nrf2 pathway.
In this study, we investigated the role of HMGB1 from melanocytes in the response to oxidative stress and the mechanism involved. We showed that HMGB1 is expressed by primary normal human epidermal melanocytes (NHEMs). H2 O2 treatment increased cytoplasmic translocation and extracellular release of HMGB1. HMGB1 knockdown by small interfering RNA (siRNA) led to decreased apoptosis of NHEMs. HMGB1 inhibition enhanced the expression of Nrf2 and its target genes. The expression of Nrf2 and its downstream antioxidant genes was downregulated after the supernatant of H2 O2 -treated NHEMs was added to HMGB1-deficient cells. HMGB1 ...
Source: J Cell Mol Med - October 19, 2018 Category: Molecular Biology Authors: Mou K, Liu W, Miao Y, Cao F, Li P Tags: J Cell Mol Med Source Type: research

Aspirin induces Nrf2-mediated transcriptional activation of haem oxygenase-1 in protection of human melanocytes from H2 O2 -induced oxidative stress.
Abstract The removal of hydrogen peroxide (H2 O2 ) by antioxidants has been proven to be beneficial to patients with vitiligo. Aspirin (acetylsalicylic acid, ASA) has antioxidant activity and has great preventive and therapeutical effect in many oxidative stress-relevant diseases. Whether ASA can protect human melanocytes against oxidative stress needs to be further studied. Here, we investigated the potential protective effect and mechanisms of ASA against H2 O2 -induced oxidative injury in human melanocytes. Human melanocytes were pre-treated with different concentrations of ASA, followed by exposure to 1.0 mM H...
Source: J Cell Mol Med - March 10, 2016 Category: Molecular Biology Authors: Jian Z, Tang L, Yi X, Liu B, Zhang Q, Zhu G, Wang G, Gao T, Li C Tags: J Cell Mol Med Source Type: research