白芍总苷对小鼠慢性皮炎-湿疹的治疗作用及其部分机制

目的研究白芍总苷(TGP)对小鼠慢性皮炎-湿疹的治疗作用及其机制。方法采用二硝基氯苯(DNCB)诱导小鼠慢性皮炎-湿疹模型,用电子天平称耳片重量,千分卡尺测定耳中部的厚度,分别计算左右耳重量差及厚度差;光镜观察小鼠耳组织病理学改变;血清IL-2和IL-4含量的测定采用放射免疫测定法。结果TGP能有效减轻慢性皮炎-湿疹小鼠耳组织肿胀,改善其病理学改变,升高其降低的IL-2水平,降低其升高的IL-4水平。结论TGP对小鼠慢性皮炎-湿疹有治疗作用,其作用机制可能与调节Th1和Th2平衡有关。     

甘草酸二铵磷脂复合物凝胶治疗小鼠慢性皮炎-湿疹的药效学研究

目的 研究甘草酸二铵磷脂复合物(diammonium glycyrrhizinate phospholipid complex,DG-PC)凝胶对小鼠慢性-皮炎湿疹的治疗作用。方法 采用2,4-二硝基氯苯对小鼠腹部致敏和耳部激发建立慢性皮炎-湿疹模型,千分尺测定右耳中部厚度,分析天平称左右耳片重量,分别计算右耳厚度差和左右耳重量差;光镜下观察小鼠耳组织的病理学变化,采用Image-pro Plus软件统计淋巴细胞数。结果 DG-PC凝胶可有效减轻慢性皮炎-湿疹小鼠耳组织肿胀度,减少淋巴细胞浸润,并能够改善其病理学改变,中剂量组凝胶效果更显著。结论 DG-PC凝胶对小鼠慢性皮炎-湿疹具有治疗作用,该作用非剂量依赖性。     

克癌新丸对小鼠肝癌H22移植瘤生长及免疫的影响

目的：探讨克癌新丸对小鼠肝癌H₂₂移植瘤生长的抑制作用及对荷瘤小鼠免疫的影响。方法：在ICR小鼠右腋皮下注射小鼠肝癌H₂₂细胞,建立小鼠移植性肿瘤模型,通过瘤重计算抑瘤率,观察克癌新丸对H₂₂移植瘤生长的抑制作用;采用腹腔巨噬细胞吞噬试验、淋巴细胞转化试验、Elisa法测定血清细胞因子TNF-α、IL-2、IL-12的水平及利用Western-blot检测瘤组织中IL-2、TNF-α的蛋白表达,观察克癌新丸对H₂₂移植瘤小鼠免疫的影响。结果：在200,400,800 mg· kg^-1时克癌新丸对H₂₂的抑瘤率分别为23.12%,38.71%和48.92%,且能提高H₂₂移植瘤小鼠的胸腺和脾指数;克癌新丸能增强H22移植瘤小鼠腹腔巨噬细胞的吞噬功能,促进淋巴细胞转化,提高血清细胞因子TNF-α、IL-2、IL-12的水平,上调瘤组织中IL-2、TNF-α的蛋白表达。结论：克癌新丸明显抑制H₂₂移植瘤的生长,具有较强的体内抗肿瘤活,其机制可能与增强移植瘤小鼠的免疫有关。     

中药川贝对哮喘模型小鼠气道重塑及TGF-β1/Smad信号通路的影响

目的：观察中药川贝对哮喘模型小鼠气道重塑及转化生长因子-β1（TGF-β1）/Smad信号通路的影响,探讨其治疗哮喘的作用机制。方法：BALB/c小鼠,随机分为正常组、模型组、高剂量组、低剂量组、阳性对照组。除正常组外,其他各组用卵蛋白（OVA）建立小鼠哮喘模型。造模成功后高剂量组和低剂量组分别按18.0 mg·kg^-1和9.0 mg·kg^-1剂量给予中药川贝灌胃;阳性对照组雾化吸入0.5 mg·kg^-1地塞米松;正常组和模型组等量生理盐水灌胃,每天 1次,连续28 d。观察各组小鼠支气管管壁厚度和平滑肌厚度的变化以及支气管肺泡灌洗液（BALF）中嗜酸性粒细胞（EOS）计数的变化;酶联免疫吸附剂测定（ELISA）检测BALF和血清中TGF-β1浓度;蛋白印记分析（Western-blot）检测肺组织TGF-β1、磷酸化Smad2（p-Smad2）、Smad2、磷酸化Smad3（p-Smad3）、Smad3的表达;实时荧光定量PCR（Real Time-PCR）检测肺组织TGF-β1 mRNA、Smad2 mRNA、Smad3 mRNA的表达。结果：模型组小鼠支气管管壁厚度和平滑肌厚度,BALF中EOS计数,BALF和血清中TGF-β1浓度,肺组织TGF-β1、p-Smad2、Smad2、p-Smad3、Smad3的表达,肺组织TGF-β1 mRNA、Smad2 mRNA、Smad3 mRNA的表达均明显高于对照组（P<0.01）,高剂量组,低剂量组和阳性对照组上述指标则明显低于模型组（P<0.05或P<0.01）。结论：中药川贝可改善哮喘模型小鼠气道重塑状态,其机制可能与其抑制TGF-β1/Smad信号通路有关。     

吡格列酮对合并代谢综合征的非酒精性脂肪性肝病患者血清TNF-α、IL-6的影响及意义

目的:研究吡格列酮对合并代谢综合征(MS)的非酒精性脂肪性肝病(NAFLD)患者血清肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)水平的影响及其意义。方法:连续收集2012年1月-2013年6月在长江航运总医院治疗的合并MS的NAFLD患者。患者分别接受非药物治疗(中等程度热量限制和中等量有氧运动)或吡格列酮(30 mg·d^-1)联合非药物治疗6个月。比较治疗后2组病例的TNF-α、IL-6、NAFLD/MS相关指标和疗效的差异,并分析TNF-α、IL-6与胰岛素抵抗指数(HOMA-IR)、疗效之间的关系。结果:共收集合并MS的HAFLD患者64例,每组各32例。非药物组治疗后6个月仅体重指数和空腹胰岛素显著性降低(P<0.05),吡格列酮联合非药物组治疗后TNF-α、IL-6水平及NAFLD/MS指标均显著改善(P<0.05)。联合治疗组的总有效率显著优于非药物组(81.3% vs 21.9%)。患者治疗前后血清TNF-α和IL-6水平差值与HOMA-IR差值显著性正相关(分别为r=0.676,P<0.001;r=0.498,P<0.001);HOMA-IR差值与疗效级别亦呈显著性正相关(r=0.608,P<0.001)。结论:吡格列酮可有效降低合并MS的NAFLD患者血清TNF-α、IL-6水平。TNF-α、IL-6可能通过影响胰岛素敏感性参与病变治疗过程。     

青蒿治疗难治性类风湿关节炎患者的疗效及对TH17/Treg细胞因子的影响

目的：探讨青蒿治疗难治性类风湿关节炎（rheumatoid arthritis,RA）患者的疗效及是否可纠正Th17/Treg失衡及对细胞因子的影响。方法：病例来源于某院风湿免疫科,64例难治性RA患者纳入,17例难治性RA患者继续应用MTX为对照组,23例难治性RA患者应用青蒿为青蒿治疗组,24例难治性RA患者应用TNFi拮抗剂+MTX为阳性对照组。予观察3组第0,4,8,12周疗效,ELISA法检测患者血清细胞因子水平IL-10、IL-17和TNF-α表达情况;多参数流式细胞术检测各组患者外周血Treg和Th17细胞表达水平。结果：（1）青蒿治疗组和阳性对照组第8周起疗效比MTX对照组对比有统计学意义;阳性对照组第4周起比青蒿治疗组效果有统计学意义;（2）青蒿治疗组和阳性对照组患者第8周血清IL-10浓度显著高于MTX组;青蒿治疗组和阳性对照组患者血清IL-17浓度显著低于MTX组。此外,青蒿治疗组和阳性对照组患者TNF-α、ESR和CRP浓度显著低于MTX组;（3）流式细胞仪检测示青蒿治疗组和阳性对照组患者Treg细胞百分比显著高于MTX组;青蒿治疗组和阳性对照组患者血清Th17细胞百分比显著低于MTX组。结论：青蒿治疗难治性类风湿关节炎患者效果明显优于MTX,但效果较TNFi拮抗剂+MTX差,其抑制炎性因子的机制可能通过纠正RA患者的TH17/Treg失衡达到治疗目的。     

沙利度胺对慢性充血性心力衰竭的影响

目的:探讨慢性充血性心力衰竭(CHF)病人应用沙度胺,治疗前后血浆心衰相关细胞因子水平及左室收缩功能变化。方法:将98例CHF病人(左室射血分数LVEF≤40％)随机分为2组,对照组常规应用治疗心衰药物,沙利度胺组在此基础上加用沙利度胺25～150mg·d-1,共用12wk,于治疗前后分别测定TNF-α,IL-6,超声心动图评价左室收缩功能。结果:CHF病人经沙利度胺治疗12wk后, TNF-α(p<0.01)、IL-6(P<0.05)水平均降低,且左室收缩功能显著改善(P<0.01)。结论:常规治疗慢性充血性心力衰竭基础上加用沙利度胺,安全易耐受,可显著改善CHF相关的临床症状和心功能。     

沙利度胺对胶原诱导型关节炎大鼠关节炎症的抑制作用及其机制探讨

目的研究沙利度胺对胶原诱导型关节炎大鼠的关节炎症及血浆血管内皮生长因子(VEGF)表达的影响。方法采用胶原诱导型关节炎(CIA)大鼠为动物模型,经给予沙利度胺治疗,测定不同时间点大鼠的足爪厚度、血浆VEGF浓度,进行踝关节病理评分和放射学检查,并与正常对照组、单纯造模组、甲氨蝶呤治疗组相比较。结果沙利度胺可以有效减轻CIA大鼠足爪肿胀程度,降低血浆VEGF浓度,疗效与甲氨蝶呤相似。结论沙利度胺可以通过影响VEGF的表达,抑制滑膜炎症及周围组织破坏,有效减轻CIA大鼠关节的炎症程度。     

火麻仁油与海藻油混合物对氧化性低密度脂蛋白诱导的内皮细胞损伤的分子保护机制研究

目的：探讨由植物来源的多不饱和脂肪酸火麻仁油与海藻油混合而成的混合物（简称AH）对氧化性低密度脂蛋白（ox-LDL）诱导的内皮细胞损伤的保护作用。方法：用ox-LDL刺激人脐静脉内皮细胞株（HUVEC-12）建立内皮细胞损伤模型，药物干预后检测细胞内NO含量，流式细胞仪检测ROS变化，TUNEL法检测细胞凋亡，RT-PCR方法检测IL-6、TNF-α、NF-κB、pAMPK、SIRT1的基因表达水平，Western-Blot方法检测P-IκB、pAMPK、SIRT1蛋白表达水平。结果：与模型组相比，多不饱和脂肪酸混合物AH可以显著减少细胞NO合成，减少ROS生成，抑制细胞凋亡，降低IL-6、TNF-α、NF-κB水平，增加pAMPK、SIRT1水平。结论：AH能够通过降低内皮炎症因子来对抗ox-LDL诱导的内皮损伤，其作用机制可能与AMPK/SIRT1/NF-κB信号通路有关。     

汉族、维吾尔族抗结核药物性肝损害患者血清TNF-α表达水平的研究

目的：探讨汉族、维吾尔族抗结核药物导致的肝损害患者血清TNF-α表达量,比较两民族间的遗传差异。并分析TNF-α表达量与肝损伤程度的关联及其临床意义。方法：服用抗结核药物导致的肝损害患者235例（汉族100例,维吾尔族135例）,ELISA法测定血清中TNF-α的含量。结果：汉族、维吾尔族肝损患者血清TNF-α表达量分别为：（31.55±12.35）,（35.92±14.59）pg·mL^-1;汉族人群轻度、中度及重度肝损伤患者血清TNF-α水平分别为：（29.35±9.35）,（30.46±10.61）,（32.95±12.35）pg·mL^-1。维吾尔族人群轻度、中度及重度肝损伤患者血清TNF-α水平分别为：（32.92±14.59）,（35.12±11.58）,（37.30±10.92）pg·mL^-1。结论：抗结核药物导致肝损伤患者血清TNF-α表达量随肝损害的严重程度增加而升高。血清TNF-α表达量维吾尔族患者显著高于汉族人群,两民族人群间存在的差异有统计学意义。     

阿魏酸对痴呆小鼠脑内胶质细胞活化与炎性细胞因子表达的影响

目的:探究阿魏酸(FA)对阿尔茨海默病(AD)模型小鼠脑内炎症与胶质细胞活化及细胞因子表达的影响,揭示阿魏酸对小鼠大脑的保护作用及其机制。方法:将50只昆明种小鼠随机分为假手术组、AD模型组、FA低、中和高3个剂量组。采用脑定位向小鼠右侧海马CA1区注射1μL Aβ1-40建立AD模型,造模成功后第3天开始给药,阿魏酸低、中、高剂量组分别按20.0、40.0、80.0mg·kg-1剂量灌胃,假手术与模型组灌胃等体积生理盐水,用药时间为30 d。实验结束后,处死动物,剖取各组小鼠大脑,采用免疫荧光方法观察大脑皮层区GFAP的表达,用ELISA法测定脑组织中IL-1β、IL-6和TNF-α含量。结果:与假手术组相比,AD模型组小鼠大脑皮层区GFAP阳性细胞表达明显增多(P<0.01),且大脑组织中IL-1β、IL-6和TNF-α含量显著升高(P<0.01、P<0.01、P<0.01);与模型组相比,阿魏酸3个剂量组小鼠皮层区域GFAP阳性细胞表达均明显减少(P<0.01),且大脑组织中IL-1β、IL-6和TNF-α含量也相应地减少(P<0.01、P<0.01、P<0.01)。结论:阿魏酸可能是通过抑制Aβ1-40对神经细胞的毒性和诱导小胶质细胞活化,使得胶质细胞合成的炎性细胞因子含量减少,进而减轻痴呆大脑组织中炎症的形成,从而达到治疗或改善AD患者的临床症状的目的。     

肤鲜洗剂对急性湿疹小鼠T细胞介导的细胞免疫调节作用研究

目的: 观察肤鲜洗剂对小鼠变应性接触性皮炎(allergic contact dermatitis,ACD)的影响。方法: 采用BALB/c小鼠40只,适应性喂养3 d后随机分为4组,每组10只,分别为空白对照组、模型对照组、肤鲜洗剂组、阳性药物对照组,除空白对照组外,均采用1% 2,4-二硝基氟苯(2,4-dinitrofluorobenzene,DNFB)丙酮橄榄油溶液致敏和激发小鼠皮肤,建立小鼠ACD模型,激发后12 h开始用药,连续2 d,每天给药2次。在激发后48 h分别对小鼠耳厚度及耳变应反应程度进行测量评分,计数1 min内小鼠搔抓耳部次数,小鼠耳部皮损以HE染色,观察皮肤炎性细胞浸润等病理变化情况。采用ELISA检测血清中γ干扰素(interferon gamma,IFN-γ)、白细胞介素-4(interleukin-4,IL-4)、白细胞介素-17(interleukin-17,IL-17)及白细胞介素-35(interleukin-35,IL-35)水平。结果: 与空白对照组比较,模型对照组小鼠耳厚度、耳变应反应评分、搔抓指数、血清中IL-4、IL-17水平显著升高(P＜0.05),IFN-γ、IL-35水平显著降低(P＜0.05),出现明显的ACD病理改变。与模型对照组比较,肤鲜洗剂可有效减轻小鼠的耳廓肿胀程度,降低耳变应反应评分,同时明显降低血清中IL-4、IL-17水平(P＜0.05),升高IFN-γ、IL-35水平(P＜0.05),显著改善耳部组织的病理形态。结论: 肤鲜洗剂对急性湿疹小鼠T细胞介导的细胞免疫具有一定的调节作用,可达到治疗急性湿疹的作用。     

氯霉素泼尼松搽剂治疗小鼠特应性皮炎的实验研究

目的:研究氯霉素泼尼松搽剂对小鼠急性特应性皮炎的治疗效果.方法:选取48只小鼠,分为空白组、模型组、对照组及实验低、中、高剂量组共6组,每组8只,除空白组外,其余5组小鼠均用二硝基氯苯丙酮溶液建立特应性皮炎模型,空白组、模型组给予生理盐水,对照组给予1％吡美莫司乳膏,实验组低、中、高剂量组分别给予相应浓度的氯霉素泼尼松...     

Oral administration of heat-killed Lactobacillus brevis SBC8803 ameliorates the development of dermatitis and inhibits immunoglobulin E production in atopic dermatitis model NC/Nga mice

We have previously shown that the oral administration of heat-killed Lactobacillus brevis (L. brevis) SBC8803 strain inhibits IgE production in ovalbumin (OVA)-sensitized BALB/c mice through improvement of the type-1 helper T (Th1)/Th2 balance toward Th1 dominance. Atopic dermatitis is one of the most common skin diseases and is frequently associated with elevated immunoglobulin E (IgE) antibodies against many kinds of allergens. In this study, we investigated the inhibitory effect of oral administration of L. brevis SBC8803 on the development of dermatitis and IgE elevation using the NC/Nga atopic dermatitis model mice. Male 8-week-old NC/Nga mice were sensitized by the topical application of picryl chloride to foot pads and shaved abdomen. These mice were boosted with picryl chloride by topical application onto the ears once a week for 9 weeks. The mice (n=10 per group) were fed a diet containing 0%, 0.05% or 0.5% of heat-killed L. brevis SBC8803 from 2 weeks before the first sensitization to the end of the study. Total IgE concentration in serum, clinical score, and ear thickness were periodically examined throughout the study. Finally, cytokine (interleukin (IL)-4, IL-5, IL-6, IL-10, IL-12, IFN-gamma and transforming growth factor (TGF)-beta) productions from splenocytes and Peyer's patch (PP) cells of mice were measured. Oral administration of L. brevis SBC8803 significantly inhibited IgE production and ear swelling, and suppressed the development of dermatitis in a dose-dependent manner. Immunosuppressive cytokines such as IL-10 and TGF-beta production from PP cells significantly increased in the 0.5% group compared to the control group although Th1-type and Th2-type cytokines production was not affected.     

The therapeutic effect of cimifugin on atopic dermatitis in mice and its mechanism北大核心CSCD

Aim To investigate the effects of cimifugin on mouse atopic dermatitis (AD) induced by fluorescein isothiocyanate (FITC) and further explore the mechanism of its action. Methods ICR mice were randomly divided into blank group, model group, positive group (dexamethasone),low dose group,high dose group and administration group of cimifugin. FITC solution was applied to the shaved abdomen of mice in the sensitization stage, and 0.6 % FITC solution was applied to attack the ears of mice in the stimulation stage. The administration groups were given medicine for seven consecutive days. The effects of cimifugin on body weight, thymus index and spleen index of mice were detected. Ear inflammatory cell infiltration was observed by HE staining. The ear swelling of mice was measured, and Th2 cytokines IL-5,IL-13 and the key promoter of allergy IL-33 were detected by ELISA. The epithelial barrier structural proteins, filaggrin, claudinl,occludin and E-cadherin,were detected by immunohistochemistry and Western blot. Results Compared with the blank group, the model group showed significant AD symptoms. Compared with the model group, cimifugin transdermal administration group significantly reduced ear inflammatory cell infiltration,ear swelling, IL-5,IL-13 and IL-33, and significantly increased the expression of filaggrin and occludin. Conclusions Transdermal administration of cimifugin could significantly inhibit AD in mice, and its mechanism involves repairing epithelial barrier function, restoring filaggrin and occludin, inhibiting allergy promoting factor IL-33, and finally inhibiting AD inflammation. © 2023 Publication Centre of Anhui Medical University. All rights reserved.     

Estrogen receptor α activation aggravates imiquimod-induced psoriasis-like dermatitis in mice by enhancing dendritic cell interleukin-23 secretion

Our recent study has reported that estrogen receptors (ERs) are involved in several types of allergy development. This study aims to investigate the possible relationship between ER activation and development of imiquimod-induced psoriasis-like dermatitis. A mouse model of imiquimod-induced psoriasis-like dermatitis was generated by 5 days of topical application of 5% of imiquimod cream on the back of the ear and the shaved back skin of male BALB/c mice. From the second day of applying 5% imiquimod cream, either ERα selective agonist (propylpyrazoletriol [PPT] 2.5 mg/kg) or ERβ selective agonist (diarylpropionitrile, DPN; 2.5 mg/kg) was administered orally for four consecutive days. Immediately after the final imiquimod cream application, scratching behavior was video monitored for 2 hours. The ear-swelling response was determined by comparing ear thickness before and after the final application of imiquimod cream. Twenty-four hours after the final imiquimod application, back skin tissue and auricular lymph nodes were isolated under isoflurane anesthesia. Oral administration of PPT significantly induced itch behavior and proinflammatory responses, including the levels of interleukin (IL)-17 and IL-22, whereas DPN treatment did not influence either pruritic or proinflammatory responses. In addition, IL-23 contribution by dendritic cells was identified using ER agonists on pretreated lipopolysaccharide (LPS)-stimulated murine bone marrow derived dendritic cells (BMDCs). PPT also significantly enhanced IL-23 secretion by LPS-stimulated BMDCs. Our findings indicate that the activation of ERα, but not ERβ, is directly associated with inflammatory and pruritic responses in a mouse model of the imiquimod-induced psoriasis by enhancing the secretion of IL-23 by dendritic cells.     

银翘散治疗小儿肺炎的临床研究

目的:探讨银翘散对小儿肺炎的治疗作用并对其机制进行研究。方法:收集某院肺炎患儿160例,均满足诊断标准,按完全随机法均分为观察组和对照组,分别以各组方案进行相应治疗。经7 d治疗,计算2组患儿治愈的有效率,观察症状好转程度,酶联免疫(ELISA)法检测患儿治疗前及治疗后血清肿瘤坏死因子、白介素-1β、白介素-6、白介素-8(TNF-α、IL-1β、IL-6、IL-8)水平。结果:治疗7 d后,观察组患儿高热、咳嗽症状显著轻于对照组及治疗前,差异有统计学意义(P<0.05或P<0.01);观察组治愈总有效率为96.25%,显著高于对照组81.25%,差异有统计学意义(χ²=7.574,P<0.05)。治疗后观察组患儿血清各因子水平均显著低于对照组及治疗前,差异有统计学意义(P<0.05或P<0.01)。结论:银翘散对小儿肺炎有较好的治疗作用,可能与其降低TNF-α、IL-1β、IL-6、IL-8水平有关。     

他克莫司软膏对小鼠变应性接触性皮炎的疗效观察

目的：评价他克莫司软膏治疗小鼠变应性接触性皮炎的疗效。方法：使用2,4-二硝基氯苯（DNCB）诱导小鼠背部变应性接触性皮炎,制造模型成功后,将60只小鼠随机分为正常对照组、模型组、卤米松组、糠酸莫米松组、丁酸氢化可的松、他克莫司组,每组10只,分别接受相应药物的治疗。观察各组小鼠皮损炎症程度、组织病理切片炎症细胞数量改变及皮损中IL-4和IFN-γ水平的变化。结果：他克莫司软膏能有效减轻小鼠背部皮损炎症程度,减少组织病理切片炎症细胞数量,调节皮损中IL-4和IFN-γ的水平;其疗效与卤米松相当,优于糠酸莫米松及丁酸氢化可的松。结论：他克莫司软膏对小鼠变应性接触性皮炎具有明显的治疗作用。     

基于P38MAPK信号通路探讨加味黄连膏对小鼠湿疹模型的影响

目的：基于P38MAPK信号通路探讨加味黄连膏对湿疹模型小鼠模型的治疗效果。方法：BALB/c小鼠60只,采用二硝基氯苯（1-chloro-24-dinitrochloro-benzene,DNCB）建立皮肤湿疹模型,随机分为6组,分别为空白对照组、空白基质（模型对照组）、复方醋酸地塞米松软膏（阳性对照组）及高、中、低剂量组（加味黄连膏治疗组）,对湿疹部位皮肤连续涂抹给药11d,以HE染色实验结果评价皮肤中炎症细胞浸润情况;Western Blot检测小鼠皮肤组织中p-p38和p38蛋白表达;qRT-PCR法检测皮肤组织中p38MAPKmRNA的表达;ELISA法检测血清中促炎细胞因子白细胞介素-6（interleukin 6,IL-6）、肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）、白细胞介素-2（interleukin 2,IL-2）、干扰素（IFN-γ）的水平。结果：药物治疗组与模型对照组相比,小鼠皮肤肿胀明显减轻;与模型对照组比较,血清中细胞因子（IL-2,IL-6,TNF-α和IFN-γ）的水平,加味黄连膏治疗组各组细胞因子水平均低于模型组（P<0.05,P<0.01）;且与模型组相比,加味黄连膏治疗组皮肤组织中p-p38MAPK蛋白水平明显下降,p-p38MAPK mRNA表达降低（P<0.05,P<0.01）。结论：加味黄连膏可以通过抑制p38MAPK信号通路的激活,抑制炎症反应,有效治疗皮炎湿疹。