中华皮肤科杂志
中華皮膚科雜誌
중화피부과잡지
Chinese Journal of Dermatology
2013年
4期
275-278
,共4页
孟晨阳%陈红光%孟啸寅%邢卫斌%付国俊
孟晨暘%陳紅光%孟嘯寅%邢衛斌%付國俊
맹신양%진홍광%맹소인%형위빈%부국준
目的 探讨饱和氢氯化钠溶液对变应性接触性皮炎(ACD)的治疗作用及相关机制.方法 将40只小鼠随机分为四组:对照组、对照+饱和氢氯化钠溶液组、ACD组和ACD+饱和氢氯化钠溶液组.将二硝基氟苯搽在小鼠外耳建立二硝基氟苯致小鼠变应性接触性皮炎模型,腹腔注射饱和氢氯化钠溶液5 ml/kg进行治疗.评估皮损,计算耳厚度差、耳肿胀度,酶联免疫吸附试验检测皮损组织肿瘤坏死因子α(TNF-α)、白介素(IL)-6、IL-17和干扰素γ(IFN-γ)水平,并计数皮损中炎性细胞数量.采用SPSS 18.0统计软件进行数据分析,各组间比较采用单因素方差分析,两两比较采用LSD分析法.结果 与对照组比较,ACD组皮损评分(7.33±1.53)、耳厚度差[(0.73±0.15) mm]和耳肿胀度[(18.67±3.05) mg]增加,左耳皮损组织TNF-α[(1475.52±233.81) ng/g]、IL-6[(184.65±78.39) ng/g]、IL-17[(628.56±201.44) ng/g]和IFN-γ[(197.72±37.81) ng/g]水平和炎性细胞数量[(752.00±166.06)个/mm2]亦增加(均P＜ 0.05)；与ACD组比较,ACD+饱和氢氯化钠溶液组皮损评分(3.33±0.58)、耳厚度差[(0.46±0.11) mm]、耳肿胀度[(11.00±2.64) mg]、左耳皮损组织TNF-α[(817.72±101.13) ng/g]、IL-6[(95.86±36.65) ng/g]、IL-17 [(373.38±126.74) ng/g]和IFN-γ[(63.31±17.38) ng/g]水平和炎性细胞数量[(384.00±97.35)个/mm2]均降低(均P＜ 0.05).结论 饱和氢氯化钠可以减轻ACD中炎症因子的释放.
目的 探討飽和氫氯化鈉溶液對變應性接觸性皮炎(ACD)的治療作用及相關機製.方法 將40隻小鼠隨機分為四組:對照組、對照+飽和氫氯化鈉溶液組、ACD組和ACD+飽和氫氯化鈉溶液組.將二硝基氟苯搽在小鼠外耳建立二硝基氟苯緻小鼠變應性接觸性皮炎模型,腹腔註射飽和氫氯化鈉溶液5 ml/kg進行治療.評估皮損,計算耳厚度差、耳腫脹度,酶聯免疫吸附試驗檢測皮損組織腫瘤壞死因子α(TNF-α)、白介素(IL)-6、IL-17和榦擾素γ(IFN-γ)水平,併計數皮損中炎性細胞數量.採用SPSS 18.0統計軟件進行數據分析,各組間比較採用單因素方差分析,兩兩比較採用LSD分析法.結果 與對照組比較,ACD組皮損評分(7.33±1.53)、耳厚度差[(0.73±0.15) mm]和耳腫脹度[(18.67±3.05) mg]增加,左耳皮損組織TNF-α[(1475.52±233.81) ng/g]、IL-6[(184.65±78.39) ng/g]、IL-17[(628.56±201.44) ng/g]和IFN-γ[(197.72±37.81) ng/g]水平和炎性細胞數量[(752.00±166.06)箇/mm2]亦增加(均P＜ 0.05)；與ACD組比較,ACD+飽和氫氯化鈉溶液組皮損評分(3.33±0.58)、耳厚度差[(0.46±0.11) mm]、耳腫脹度[(11.00±2.64) mg]、左耳皮損組織TNF-α[(817.72±101.13) ng/g]、IL-6[(95.86±36.65) ng/g]、IL-17 [(373.38±126.74) ng/g]和IFN-γ[(63.31±17.38) ng/g]水平和炎性細胞數量[(384.00±97.35)箇/mm2]均降低(均P＜ 0.05).結論 飽和氫氯化鈉可以減輕ACD中炎癥因子的釋放.
목적 탐토포화경록화납용액대변응성접촉성피염(ACD)적치료작용급상관궤제.방법 장40지소서수궤분위사조:대조조、대조+포화경록화납용액조、ACD조화ACD+포화경록화납용액조.장이초기불분차재소서외이건립이초기불분치소서변응성접촉성피염모형,복강주사포화경록화납용액5 ml/kg진행치료.평고피손,계산이후도차、이종창도,매련면역흡부시험검측피손조직종류배사인자α(TNF-α)、백개소(IL)-6、IL-17화간우소γ(IFN-γ)수평,병계수피손중염성세포수량.채용SPSS 18.0통계연건진행수거분석,각조간비교채용단인소방차분석,량량비교채용LSD분석법.결과 여대조조비교,ACD조피손평분(7.33±1.53)、이후도차[(0.73±0.15) mm]화이종창도[(18.67±3.05) mg]증가,좌이피손조직TNF-α[(1475.52±233.81) ng/g]、IL-6[(184.65±78.39) ng/g]、IL-17[(628.56±201.44) ng/g]화IFN-γ[(197.72±37.81) ng/g]수평화염성세포수량[(752.00±166.06)개/mm2]역증가(균P＜ 0.05)；여ACD조비교,ACD+포화경록화납용액조피손평분(3.33±0.58)、이후도차[(0.46±0.11) mm]、이종창도[(11.00±2.64) mg]、좌이피손조직TNF-α[(817.72±101.13) ng/g]、IL-6[(95.86±36.65) ng/g]、IL-17 [(373.38±126.74) ng/g]화IFN-γ[(63.31±17.38) ng/g]수평화염성세포수량[(384.00±97.35)개/mm2]균강저(균P＜ 0.05).결론 포화경록화납가이감경ACD중염증인자적석방.
Objective To evaluate the therapeutic effect of hydrogen-rich saline on allergic contact dermatitis (ACD) in mice and to explore its underlying mechanisms.Methods Forty mice were equally divided into 4 groups:control group,control treatment group,ACD group and ACD treatment group.ACD was induced by repetitive topical application of dinitrofluorobene (DNFB) to the left ear of mice on day 1,2 and 5.Hydrogen-rich saline was intraperitoneally given to the mice in the ACD treatment group at a dose of 5 ml/kg per day from day 1 to 5.On day 6,the mice were sacrificed,ear tissue was removed from them and subjected to measurement of thickness and weight,detection of tumor necrosis factor (TNF)-α,interleukin (IL)-6,IL-17 and interferon (IFN)-γ expression by enzyme linked immunosorbent assay,as well as numeration of inflammatory cells in lesions after hematoxylin-eosin (HE) staining.Data were processed by SPSS 18.0 software,and statistical analysis was carried out by one-way analysis of variance and least significant difference (LSD) procedure.Results Compared with the control group,the ACD group showed a significant increase in lesion score (7.33 ± 1.53 vs.0,P ＜ 0.05),differences in the thickness ((0.73 ± 0.15) mm vs.(0.13 ± 0.05) mm,P ＜ 0.05) and swelling degree (expressed as tissue weight:(18.67 ± 3.05) mg vs.(3.33 ± 1.52) mg,P ＜ 0.05) between the left and right ear,expressions of TNF-α ((1475.52 ± 233.81) pg/mg vs.(239.01 ± 52.39) pg/mg,P＜ 0.05),IL-6 ((184.65 ± 78.39) pg/mg vs.(42.28 ± 17.64) pg/mg,P＜ 0.05),IL-17 ((628.56 ± 201.44) pg/mg vs.(127.58 ± 50.28) pg/mg,P＜ 0.05) and IFN-γ ((197.72 ± 37.81) pg/mg vs.(24.57 ± 8.31) pg/mg,P ＜ 0.05),and the number of inflammatory cells per square millimetre in the left ear tissue (752.00 ± 166.06 vs.127.33 ± 77.18,P ＜ 0.05).However,hydrogen-rich saline treatment induced a statistical decrease in all of these parameters in the ACD treatment group compared with the ACD group,including lesion score (3.33 ± 0.58,P ＜ 0.05),difference in thickness ((0.46 ± 0.11) mm,P ＜ 0.05) and swelling degree ((11.00 ± 2.64) mg,P ＜ 0.05),expressions of TNF-α ((817.72 ± 101.13) pg/mg,P＜ 0.05),IL-6 ((95.86 ± 36.65) pg/mg,P＜ 0.05),IL-17 ((373.38 ± 126.74) pg/mg,P＜ 0.05),IFN-γ ((63.31± 17.38) pg/mg,P ＜ 0.05) and the number of inflammatory cells per square millimetre (384.00 ± 97.35,P ＜0.05).Conclusion Hydrogen may inhibit the release of inflammatory factors in ACD.
