“…In the present study, we initially found that EGb761 showed no toxic effect on PIG1 cells (data not shown), which was consistent with previous studies . The patients with vitiligo have inferior capacity against oxidative stress due to the lower activity of SOD and GSH‐Px . Our study showed that EGb761 could significantly restore the activity of SOD and GSH‐Px in PIG1 cells under H 2 O 2 treatment.…”
Section: Discussionsupporting
confidence: 93%
“…10 The patients with vitiligo have inferior capacity against oxidative stress due to the lower activity of SOD and GSH-Px. 20,21 Our study showed that EGb761 could significantly restore the activity of SOD and GSH-Px in PIG1 cells under H 2 O 2 treatment.…”
Vitiligo is a common skin depigmenting disorder characterized by the loss of functional melanocytes. Its pathogenesis is complicated and oxidative stress plays a critical role in the development of vitiligo. Thus, antioxidant therapy is a promising therapeutic strategy to prevent or even reverse the progression of depigmentation. Ginkgo biloba extract EGb761 has been confirmed to have protective effects on neurons against oxidative stress. Notably, several clinical trials have shown that patients with stable vitiligo achieved repigmentation after taking EGb761. However, the exact mechanism underlying the protective effects of EGb761 on melanocytes against oxidative stress has not been fully elucidated. In the present study, we found that EGb761 effectively protected melanocytes against oxidative stress‐induced apoptosis and alleviated the excessive accumulation of reactive oxygen species (ROS) and lipid peroxidation by enhancing the activity of antioxidative enzymes. Furthermore, the antioxidative effect of EGb761 was achieved by activating Nrf2 and its downstream antioxidative genes. In addition, interfering Nrf2 with siRNA abolished the protective effects of EGb761 on melanocytes against oxidative damage. In conclusion, our study proves that EGb761 could protect melanocytes from H
2
O
2
‐induced oxidative stress by activating Nrf2. Therefore, EGb761 is supposed to be a potential therapeutic agent for vitiligo.
“…In the present study, we initially found that EGb761 showed no toxic effect on PIG1 cells (data not shown), which was consistent with previous studies . The patients with vitiligo have inferior capacity against oxidative stress due to the lower activity of SOD and GSH‐Px . Our study showed that EGb761 could significantly restore the activity of SOD and GSH‐Px in PIG1 cells under H 2 O 2 treatment.…”
Section: Discussionsupporting
confidence: 93%
“…10 The patients with vitiligo have inferior capacity against oxidative stress due to the lower activity of SOD and GSH-Px. 20,21 Our study showed that EGb761 could significantly restore the activity of SOD and GSH-Px in PIG1 cells under H 2 O 2 treatment.…”
Vitiligo is a common skin depigmenting disorder characterized by the loss of functional melanocytes. Its pathogenesis is complicated and oxidative stress plays a critical role in the development of vitiligo. Thus, antioxidant therapy is a promising therapeutic strategy to prevent or even reverse the progression of depigmentation. Ginkgo biloba extract EGb761 has been confirmed to have protective effects on neurons against oxidative stress. Notably, several clinical trials have shown that patients with stable vitiligo achieved repigmentation after taking EGb761. However, the exact mechanism underlying the protective effects of EGb761 on melanocytes against oxidative stress has not been fully elucidated. In the present study, we found that EGb761 effectively protected melanocytes against oxidative stress‐induced apoptosis and alleviated the excessive accumulation of reactive oxygen species (ROS) and lipid peroxidation by enhancing the activity of antioxidative enzymes. Furthermore, the antioxidative effect of EGb761 was achieved by activating Nrf2 and its downstream antioxidative genes. In addition, interfering Nrf2 with siRNA abolished the protective effects of EGb761 on melanocytes against oxidative damage. In conclusion, our study proves that EGb761 could protect melanocytes from H
2
O
2
‐induced oxidative stress by activating Nrf2. Therefore, EGb761 is supposed to be a potential therapeutic agent for vitiligo.
Background:Oxidative stress is considered as an initial pathogenic event in melanocyte destruction. These free radicals are scavenged by antioxidants, whose sum of activity in serum is measured by total antioxidant status (TAS). In addition, homocysteine (Hcy) may mediate melanocyte destruction via increased oxidative damage. However, previous studies investigating these parameters in vitiligo provide equivocal results.Aims:To study and compare serum Hcy and TAS levels in vitiligo patients with controls and also to correlate these parameters with the various disease characteristics. The present study further looked into any correlation between serum Hcy and TAS in vitiligo.Materials and Methods:A case control study was conducted on 82 vitiligo patients and 83 controls aged 18–45 years after excluding factors which could potentially alter serum Hcy or TAS levels. Disease characteristics were studied and blood samples were obtained for measuring serum Hcy and TAS levels.Results:TAS levels were lower in vitiligo patients than controls (1.79 ± 0.51 vs. 2.16 ± 0.63 mmol/L; P < 0.001) and had a negative correlation with disease activity (r = −0.410, P < 0.001). However, serum Hcy levels were comparable between vitiligo patients (18.68 ± 9.90 μmol/L) and controls (20.21 ± 13.39 μmol/L) (P = 0.406). No significant correlation was found between serum Hcy and serum TAS levels.Conclusions:Serum TAS may be further investigated to establish its role as biomarker for vitiligo since its levels also correlate with disease activity. However, serum Hcy may not be a reliable marker in Indian population probably because of differences in dietary habits.
“…Conflicting data have been reported about GPx levels in vitiligo patients, with a recent meta-analysis finding that GPx levels were decreased in Asian, but not white, vitiligo patients (Xiao et al, 2016). However, a study of 60 vitiligo patients found decreased GPx activity levels when compared with control subjects and a statistically significant decrease in GPx in patients with dark skin phenotypes (skin types IV and V) when compared with lighter skin types (skin type III) (Zedan et al, 2015). Thus, lower levels of GPx in women with darker skin phenotypes, which would include those with increased tanning ability, may confer a greater vitiligo risk.…”
Vitiligo is the most common cutaneous depigmentation disorder worldwide, yet little is known about specific risk factors for disease development. Using data from the Nurses' Health Study, a prospective cohort study of 51,337 white women, we examined the associations between (i) pigmentary traits and (ii) reactions to sun exposure and risk of incident vitiligo. Nurses' Health Study participants responded to a question about clinician-diagnosed vitiligo and year of diagnosis (2001 or before, 2002-2005, 2006-2009, 2010-2011, or 2012+). We used Cox proportional hazards regression models to estimate the multivariate-adjusted hazard ratios and 95% confidence intervals of incident vitiligo associated with exposures variables, adjusting for potential confounders. We documented 271 cases of incident vitiligo over 835,594 person-years. Vitiligo risk was higher in women who had at least one mole larger than 3 mm in diameter on their left arms (hazard ratio = 1.37, 95% confidence interval = 1.02-1.83). Additionally, vitiligo risk was higher among women with better tanning ability (hazard ratio = 2.59, 95% confidence interval = 1.21-5.54) and in women who experienced at least one blistering sunburn (hazard ratio = 2.17, 95% confidence interval = 1.15-4.10). In this study, upper extremity moles, a higher ability to achieve a tan, and history of a blistering sunburn were associated with a higher risk of developing vitiligo in a population of white women.
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