Vitamin D receptor gene polymorphism, serum 25-hydroxyvitamin D levels, and risk of vitiligo: A meta-analysis.

OBJECTIVES: To explore the relationship among the vitamin D receptor (VDR) gene polymorphisms, serum 25-hydroxyvitamin D levels, and vitiligo. METHODS: Databases including PubMed, Cochrane Library, Ovid, Web of Science, CNKI, SinoMed, and Wanfang Data were systematically searched. The association was assessed using odds ratios (ORs), standard mean difference (SMD), and 95% confidence intervals (CIs). The statistical tests were performed using Review Manager 5.3.3. RESULTS: We identified a total of 17 studies. The relationship between VDR gene polymorphisms (BsmI, ApaI, TaqI, and FokI), serum 25 (OH)D levels, and incidence of vitiligo was investigated. The results of this meta-analysis showed that the dominant genetic model (CC+AC vs AA, P = .007, OR = 1.41, 95% CI = 1.10-1.80), recessive genetic model (CC vs AC+AA, P = .01, OR = 4.10, 95% CI = 1.36-12.35), and allelic contrast model (C vs A, P = .005, OR = 1.87, 95% CI = 1.21-2.90) of VDR Apal locus increased the risk of vitiligo, and BsmI, TaqI, and FokI loci and the risk of vitiligo have no obvious correlation. Serum 25 (OH)D deficiency was positively associated with the incidence of vitiligo (P < .0001, SMD = -0.94, 95% CI = -1.39, -0.48). CONCLUSION: This meta-analysis revealed that VDR Apal polymorphism increased the susceptibility risk of vitiligo, and there is a positive correlation between serum 25 (OH)D deficiency and the incidence of vitiligo.

Naringenin protects keratinocytes from oxidative stress injury via inhibition of the NOD2-mediated NF-κB pathway in pemphigus vulgaris.

Naringenin is known to have anti-oxidative activity; however, the effect of naringenin on the progression of pemphigus vulgaris (PV) still remains unclear. This study aims to analyze the effect of naringenin on HaCaT cell apoptosis and oxidative damage under the treatment of PV serum. The results showed that PV serum significantly induced cell apoptosis compared with the control group; whereas, comparing with PV group, naringenin inhibited cell apoptosis. Moreover, PV serum increased the expression of bax and caspase-3, and decreased the expression of bcl-2; but naringenin significantly suppressed the expression of bax and caspase-3, induced the expression of bcl-2. Naringenin inhibited PV serum-induced disruption of cell-cell contacts. Naringenin also down-regulated the expression of Dsg1, Dsg3 and E-cadherin compared with the PV group. Additionally, naringenin noticeably decreased the PV serum-induced ROS production and alleviated PV serum induced the drop of mitochondrial membrane potential. Furthermore, naringenin increased the activity of SOD, GSH-Px and TAC under the treatment of PV serum. Naringenin also decreased the expression of NOD2, RIPK2 and NF-κB p-p65, but this effect could be reversed by muramyl dipeptide (MDP). In conclusion, these results suggested that naringenin protected keratinocytes from apoptosis and oxidative stress injury through inhibition of the NOD2-mediated NF-κB pathway.