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Objective To evaluate the efficacy of 0.1% tacrolimus ointment and 0.1% mometasone furoate cream in the treatment of chronic actinic dermatitis (CAD). Methods Forty male patients with CAD were recruited and divided into two groups randomly.Twenty cases were treated with 0.1%tacrolimus ointment (Group A), and the other 20 cases were treated with 0.1% mometasone furoate cream (Group B) . The medications mentioned were applied topically to the lesions on the face twice a day and mizolastine tablet 10 mg per day given orally for 4 weeks. The therapeutic efficacy and side effects of medications were observed. The enzyme linked immunosorbent assay (ELISA) method was used to measure the serum levels of IFN-γ, IL-2 and IL12 in CAD patients before and after treatment with topical tacrolimus ointment and mometasone furoate cream. Results (1) Both groups had overall response rates of 100%, with no statistically significant difference ( > 0.05) . (2) Serum levels of IFN-γ,IL-2 and IL-12 were down-regulated after treatment in both treatment groups respectively ( 0.05) . Conclusion 0.1%tacrolimus ointment is effective in the treatment of CAD. Its therapeutic efficacy is equivalent to that of 0.1%mometasone furoate cream. It can be used as a possible steroid sparing equivalent.
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Objective To observe the effects of gypenosides (GP) on nuclear factor κB (NF-κB) and p38 mitogen activated protein kinase (p38MAPK) signaling pathways in photodamaged skin of mice,and to explore the mechanisms underlying the protective effects of GP against photodamage.Methods Eighty Balb/C female mice were randomly divided into 8 groups: blank control group receiving no treatment,ultraviolet B (UVB) model group receiving UVB irradiation for 60 seconds,GP group Ⅰ receiving topical GP treatment followed by UVB irradiation,GP group Ⅱ receiving UVB irradiation followed by topical GP treatment,VitE group Ⅰ receiving topical VitE treatment followed by UVB irradiation,VitE group Ⅱ receiving UVB irradiation followed by topical VitE treatment,matrix group Ⅰ receiving topical matrix treatment followed by UVB irradiation,matrix group Ⅱ receiving UVB irradiation followed by topical matrix treatment.UVB irradiation lasted 60 seconds at one time,and was given once every other day for 7 times to establish a skin model of photodamage.The interval between irradiation and topical treatment was 30 minutes in all the groups except the control group and UVB model group.After the last treatment,mice were sacrificed.Western blot was performed to measure the protein expressions of inhibitor of NF-κB(IκB),inhibitor of NF-κB kinase (IKK),p38MAPK as well as phosphorylated p38MAPK (pp38) in skin tissue from the mice.Results No expressions of IκB or IKK were observed in the blank control group.The expression level of IκB was 0.40 ± 0.07 in UVB model group,significantly lower than that in GP group Ⅰ (1.63 ± 0.85,P ＜ 0.05) and GP group Ⅱ (0.90 ± 0.40,P ＜ 0.05),whereas the level of IKK protein was higher in UVB model group than in the GP group Ⅰ and Ⅱ (2.01 ± 1.75vs.0.23 ± 0.12 and 0.45 ± 0.29,both P ＜ 0.05).No significant difference was observed in the expression of IκB or IKK proteins between the GP group Ⅰ,Ⅱ,VitE group Ⅰ and Ⅱ or in the expression of p38MAPK between the 8 groups.The phosphorylated p38MAPK expression in UVB model group was significantly higher than that in GP group Ⅰ and Ⅱ (0.835 ± 0.049 vs.0.425 ± 0.054 and 0.571 ± 0.090,both P＜ 0.05),but similar to that in VitE groups.Conclusions UVB can activate NF-κB and phosphorylated p38MAPK signaling pathways; GP 1.5％ cream can inhibit UVB-induced activation of NF-κB and p38MAPK pathways,which may be one of the mechanisms underlying its protective effects against inflammation and photodamage.
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Objective To explore the mechanism underlying the effects of gypenosides (GP) against photodamage. Methods Eighty BALB/c mice were equally divided into 8 groups, i.e., blank control group (untreated), UVB model group (irradiated with UVB), GP I group (irradiated with UVB before topical application of GP), GPⅡ group (irradiated with UVB followed by topical application of GP), VitE I group (irradiated with UVB after topical application of Vitamine E cream), VitE Ⅱ group (irradiated with UVB followed by topical application of Vitamine E cream), Vehicle group Ⅰ (irradiated with UVB after application of the drug vehicle),and Vehicle group Ⅱ (irradiated with UVB before application of the drug vehicle). UVB irradiation was performed once every other day for 14 days. Mice were sacrificed after the last irradiation and skin specimens were obtained from the irradiated sites, and the levels of p53 and p21 protein were measured by Western blot in the specimens. Results The expression level of p53 protein was significantly lower in the blank control group than in the UVB model group (0.11 ± 0.08 vs. 0.22 ± 0.12) and GP Ⅰ group (0.44 ± 0.23, P < 0.01),in the blank control group and UVB model group than in the GP Ⅱ group (0.48 ± 0.24, P < 0.01, 0.05). VitE Ⅰ group (0.49 ± 0.29) and VitE II group (0.50 ± 0.27) were similar to the GP groups in the expression of p53 protein. No statistical difference was observed in the expression of p21 protein between the eight groups. Conclusion The upregulation of p53 protein expression in epidermal cells may be related to the mechanisms underlying the protective effect of 1.5% GP cream against photodamage.
