香鳞毛蕨提取物对咪喹莫特诱导银屑病样小鼠皮损的影响

目的观察香鳞毛蕨提取物对咪喹莫特诱导银屑病样小鼠皮损的干预作用。方法采用背部每日涂抹5%咪喹莫特乳膏制作银屑病样小鼠模型。72只6~8周龄雄性BALB/c小鼠随机分为空白组、模型组、香鳞毛蕨提取物组和阳性药组,每组8只。模型组和空白组给予蒸馏水灌胃,各给药组给予相应药物灌胃,每日0.3 m L,连续6 d。采用银屑病皮损面积和严重程度指数(PASI)评分标准观察银屑病样小鼠皮损变化。光镜下观察皮损组织形态学变化,测量表皮层厚度;检测小鼠脾指数。结果与空白组比较,模型组小鼠皮肤出现鳞屑、红斑,皮损增厚;皮损组织表现为表皮棘细胞层增厚,角化不全;脾脏肥大;与模型组比较,香鳞毛蕨提取物组小鼠银屑病样皮损症状缓解,PASI积分降低,角化不全减轻,脾指数明显降低。结论香鳞毛蕨提取物可显著改善咪喹莫特诱导的小鼠银屑病样皮损。     

麻防犀角地黄汤对miR-215-5p的干预作用及对银屑病小鼠的影响

目的:通过建立银屑病小鼠模型,观察麻防犀角地黄汤对银屑病皮损及miR-215-5p的影响,探讨麻防犀角地黄汤治疗银屑病的作用机制.方法:咪喹莫特(IMQ)乳膏局部涂抹诱导建立银屑病小鼠模型,麻防犀角地黄汤灌胃干预.观察小鼠体质量、PASI评分、左耳耳廓外缘的厚度、皮损组织的病理改变;qRT-PCR法检测皮损中miR-2...     

孟根乌森乌日勒对银屑病样皮损小鼠的影响及对IL-17、IL-18、IL-22调节作用的研究

目的:观察孟根乌森乌日勒对咪喹莫特诱导的银屑病样皮损的治疗作用及其机制。方法:BALB/c雌性小鼠50只,随机分为正常对照组、模型组、孟根乌森乌日勒0.33g/kg、0.66g/kg、1.32g/kg剂量组,灌胃给药21天。采用药物诱导的方法激发小鼠皮肤出现银屑病样的变化,并通过小鼠皮肤病损的(PASI)评分来观察银屑病样小鼠模型皮损的变化情况,光镜下观察皮损组织形态学变化。用ELISA方法检测血清IL-17、IL-18、IL-22的含量。结果:咪喹莫特诱导的动物模型小鼠背部皮肤出现红斑、表皮肥厚、鳞屑成层等现象;使用孟根乌森乌日勒之后,0.33g/kg、0.66g/kg、1.32g/kg剂量组咪喹莫特银屑病模型的症状得到明显改善,银屑病样皮损减轻,PASI评分降低,角化不全现象得到改善,表皮厚度明显薄于模型对照组,其中1.32g/kg剂量组改善更加明显。血清细胞因子检测结果显示0.33g/kg、0.66g/kg、1.32g/kg剂量组IL-17、IL-18、IL-22的含量均低于模型组。结论:孟根乌森乌日勒对咪喹莫特诱导小鼠银屑病样皮损有较好的治疗作用,治疗机制是通过影响表皮细胞过度增殖、角化不全、炎症细胞浸润及血管增生而改善咪喹莫特诱导的小鼠银屑病样皮损变化。     

四妙丸调控IL-25-IL-17RA/IL-17RB对咪喹莫特诱导银屑病样小鼠模型的保护作用

目的 探讨四妙丸通过调控Interleukin(IL)-25-IL-17RA/IL-17RB轴对咪喹莫特诱导的银屑病样小鼠模型的保护作用及作用机制。方法 将30只BALB/c雄性小鼠随机分为正常组、模型组、阳性药组(甲氨蝶呤3 mg·kg^-1)、四妙丸高、低剂量组(4 g·kg^-1、2 g·kg^-1),每组6只。在等面积(2 cm×3 cm)小鼠背部皮肤上除去被毛，除正常组外其余各组小鼠涂抹咪喹莫特乳膏(62.5 mg/只);各组灌胃给予相应溶媒或受试药物，连续干预5天。期间观察并记录各组小鼠背部PASI评分。在第5天收集血清及小鼠皮肤样品，剖取脾脏计算脏器系数，HE染色观察表皮厚度，ELISA法检测各组小鼠皮损组织及血清中IL-17A、IL-25、IL-23和IL-36水平，IHC法检测各组皮肤中IL-25、IL-17RA、IL-17RB的表达水平。结果 PASI评分及HE染色结果显示，给予四妙丸后，可显著改善小鼠背部皮肤发红、增厚、皮屑增多等银屑病特征性临床表现，小鼠背部皮肤结痂及表皮增厚现象明显减轻；在皮肤组织及血...     

加味净屑饮对咪喹莫特诱导的银屑病小鼠的治疗作用及IL-17产生的影响

目的:研究加味净屑饮对咪喹莫特诱导的银屑病小鼠模型的治疗作用及IL-17产生的影响。方法:通过咪喹莫特诱导银屑病样的小鼠模型,随机分为模型组、阳性药物及加味净屑饮低剂量组(3 g/kg)、加味净屑饮中剂量组(6 g/kg)、加味净屑饮高剂量组(12 g/kg)组,另设空白对照组;游标卡尺检测左耳厚度;HE染色检测银屑病样皮损炎症状况。ELISA法测定模型小鼠血清Th17细胞细胞因子(IL-17)的表达水平。结果:加味净屑饮高剂量药物干预显著降低咪喹莫特诱导的模型小鼠左耳厚度(P<0.01),减少左耳炎症细胞的浸润,降低咪喹莫特诱导的模型小鼠血清IL-17的表达水平(P<0.05)。结论:加味净屑饮对咪喹莫特诱导的银屑病小鼠模型有较好的治疗作用,其机制可能与抑制IL-17的产生有关。     

鸦胆子苦醇对IMQ诱导的小鼠银屑病样皮损的疗效及其机制研究

目的 探究鸦胆子苦醇对balb/c小鼠银屑病模型的疗效及对相关炎症因子的影响。方法 将6-8周龄雌性balb/c小鼠随机分为：正常对照组、模型组、卡泊三醇组、鸦胆子苦醇高、中、低剂量组，n=6。小鼠背部剃毛，连续7天62.5mg IMQ涂抹造模，同上各组小鼠分别给予对应干预治疗。记录形态学变化并行PASI评分，干预结束后行常规HE染色，实时荧光定量PCR法检测组织NF-κB、CK1、CK10、TNF-α、IL-1β、IL-17的mRNA表达水平，蛋白免疫印迹法检测NF-κB、pNF-κB、CK10、TNF-α等相关蛋白表达水平。ELISA检测血清细胞因子IL-1β、IL-17、IL-6表达水平。结果 鸦胆子苦醇治疗后，小鼠银屑病样皮损明显减轻，高中低剂量组PASI评分较模型组均有明显好转(P<0.05),HE结果显示鸦胆子苦醇治疗组角质层增厚情况较模型组明显减轻，且表皮平整，表皮突恢复平整，炎症细胞浸润减轻。Real-time PCR、 Western blot及ELISA结果经治疗后相关因子均明显表达下调(P<0.001)。结论 鸦胆子苦醇有效减轻了银屑病小鼠皮损症状，这...     

银屑片治疗小鼠银屑病的实验研究

目的考察银屑片(萆薢、当归、红花、栀子等)对银屑病样小鼠模型的治疗作用。方法采用咪喹莫特诱导的小鼠银屑病样模型及鼠尾鳞片颗粒层模型,观察银屑片对皮损形态学变化及对表皮颗粒层形成的影响。结果咪喹莫特模型组小鼠皮肤出现红斑、鳞屑、皮肤增厚现象,皮损组织表现为棘层增厚、角化不全。与模型组相比,银屑片各剂量组小鼠银屑病样皮损症状减轻,银屑病皮损面积和疾病严重程度(PASI)评分降低,角化不全和表皮增厚现象得到改善,增殖细胞核抗原(PCNA)的表达有所降低。与正常对照组相比,银屑片各剂量组对小鼠鼠尾鳞片颗粒层的形成有促进作用。结论银屑片对上述小鼠银屑病模型具有一定的治疗作用。     

银屑平丸对小鼠银屑病样模型血清中TGF-β、IL-10表达的影响

目的:观察银屑平丸对BALB/c小鼠银屑病样模型血清中转化生长因子-β(TGF-β)和白细胞介素10(IL-10)表达的影响,探讨银屑平丸治疗银屑病的可能作用机制。方法:将48只BALB/c雄性小鼠随机分为空白组、模型对照组、银屑平丸高、中、低剂量组、雷公藤组,每组8只。所有小鼠背部脱毛后,空白组小鼠外涂凡士林,其余5组小鼠外涂咪喹莫特乳膏,诱发小鼠银屑病样模型;同时予以相应药物进行灌胃干预,连续8 d。观察并记录小鼠背部皮肤皮损面积和严重程度指数(psoriasis area and serenty index,PASI)评分;ELISA法检测小鼠外周血清中TGF-β、IL-10水平;取小鼠背部皮肤组织做病理切片进行组织病理观察。结果:银屑平丸高、中、低剂量组、雷公藤组小鼠背部皮损PASI评分及外周血TGF-β、IL-10含量均明显低于模型对照组,差异有统计学意义(P0.05)。结论:银屑平丸能降低银屑病样模型小鼠外周血TGF-β、IL-10的表达,这可能是银屑平丸治疗银屑病的作用机制之一。     

基于肠-免疫-皮肤轴探讨洋金花对银屑病小鼠肠道Th17/Treg轴的影响

目的探讨洋金花醉茄内酯类化合物对银屑病小鼠肠道中Th17/Treg细胞功能的影响。方法采用经典的银屑病小鼠模型,即咪喹莫特乳膏(IMQ)诱导小鼠背部皮肤产生银屑病样病理模型,并随机分为四组,即空白组、模型组、洋金花组和雷公藤阳性药物组。采用Psoriasis area and severity index(PASI)分析各组皮损严重程度;应用流式细胞法检测小鼠肠系膜淋巴结中Th17/Treg细胞数量表达;应用酶联免疫吸附法(ELISA法)依次检测肠粘膜中Th17/Treg细胞相关因子的含量。结果洋金花组能减少IMQ诱导的PASI评分,降低肠系膜中Th17细胞表达及相关细胞因子,而升高Treg细胞的表达及相关细胞因子。结论洋金花醉茄内酯类化合物可降低银屑病小鼠肠道Th17细胞功能,同时升高Treg细胞功能,进一步提示在肠-免疫-皮肤轴中,洋金花醉茄内酯类化合物通过影响肠道中的Th17/Treg细胞免疫平衡而达到防治银屑病的作用。     

银屑舒凝胶对咪喹莫特诱导银屑病模型的影响及抗炎止痒的研究

目的研究银屑舒凝胶对银屑病模型的干预作用及抗炎止痒作用。方法咪喹莫特诱导小鼠产生银屑病样损伤,以PASI评分和病理、脏器指数为评价指标研究其对银屑病干预作用;巴豆油致小鼠耳廓肿胀法计算肿胀度和肿胀抑制率研究其抗炎作用;磷酸组胺致痒法测定豚鼠的致痒阈研究其止痒作用。结果模型组小鼠皮肤增厚、长出鳞屑、表皮角化过度或不全,真皮层出现炎性浸润,使用银屑舒后,症状改善,PASI评分降低,角化不全和炎性浸润减轻,皮损厚度变薄,脾脏指数降低,其中高剂量组改善明显。中、高剂量组中止痒阈值和肿胀抑制率均升高。结论银屑舒凝胶对咪喹莫特诱导的银屑病有较好的治疗作用和抗炎止痒作用。     

Therapeutic effects of the extract of Sancao Formula,a Chinese herbal compound,on imiquimod-induced psoriasis via cysteine-rich protein 61

ObjectivePsoriasis is a common chronic inflammatory skin disease that is prone to recurrence, and the proinflammatory factor, cysteine-rich protein 61 (Cyr61), is important in its pathophysiology. Long-term clinical practice has shown that Sancao Formula (SC), a Chinese herbal compound, is effective in the treatment of psoriasis, but the precise mechanism remains unknown. In this study, we investigate the mechanism by which SC extract alleviates imiquimod (IMQ)-induced psoriasis.MethodsThe expression of Cyr61 in psoriatic lesions and normal healthy skin was detected using immunohistochemical analysis to investigate the biological role of Cyr61 in models of psoriatic inflammation. A psoriatic mouse model was established by topical application of IMQ, and the effect of topical application of SC extract was evaluated using the psoriasis area and severity index (PASI) score, hematoxylin-eosin staining, and histopathological features of the skin. Next, a HaCaT cell inflammation model was established using interferon-γ (IFN-γ), and the effect of SC extract on the mRNA and protein levels of Cyr61 and intercellular cell adhesion molecule-1 (ICAM-1) was confirmed using Western blot and quantitative real-time polymerase chain reaction analyses.ResultsImmunohistochemical staining showed that the expression of Cyr61 in psoriatic lesions was higher than that in normal skin samples (78.26% vs 41.18%, P < 0.05), and the number of Cyr61-positive cells in psoriatic lesions was also significantly higher than in normal skin (18.66 ± 2.51 vs 4.33 ± 1.52, P < 0.05). Treatment in mice with IMQ-induced psoriasis showed that SC extract could significantly improve the inflammatory phenotype, PASI score (10.875 ± 0.744 vs 3.875 ± 0.582, P < 0.05), and pathological features compared with those in IMQ model group; SC treatment was also associated with decreased levels of Cyr61 and ICAM-1. In the IFN-γ-induced inflammatory cell model, the mRNA and protein levels of Cyr61 and ICAM-1 were upregulated, while the SC extract downregulated the levels of Cyr61 and ICAM-1.ConclusionThe results provide a theoretical basis for the involvement of Cyr61 in the pathogenesis of psoriasis, and suggest that SC should be used to target Cyr61 for the prevention of psoriasis recurrence.     

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??OBJECTIVE To prepare artesunate cream and study the effect on imiquimod-induced psoriasis-like skin lesions in mice. METHODS Forty-eight mice were randomly divided into normal control group, model control group, artesunate cream in low, medium, and high dose groups and drug control group, eight mice in each group. The 5% imiquimod was used to induced psoriasis-like skin lesions model in mice. Normal control group and model control group were given blank creams, other groups were treated externally with continuous 7 d. Record the PASI score of erythema, scales, skin thickness and the PASI score was statistically analyzed by t test .The tissues of the back were paraffin embedded, sectioned and stained with HE. Observe histopathological changes of the back skin lesions in mice and calculate the histopathological scoreaccording to the histopathological score criteria. RESULTS Cumulative PASI scoreof erythema, scales, thickness showed that the group of 1% artesunate cream was significantly different compared with the model group and the group of 0.5% artesunate cream was different compared with the model group. Histopathological score showed that the groups of 0.5%, 1% artesunate cream were all different compare with the model group.CONCLUSION AST cream has a good therapeutic effect on psoriasis, and its mechanism may be related to the artesunate inhibits the proliferation of activated HaCaT cells. Artesunate cream is expected to develop a new drug for treating psoriasis.     

Antiproliferation of keratinocytes and alleviation of psoriasis by the ethanol extract of Artemisia capillaris

The therapeutic potentials of the ethanol extract of Artemisia capillaris (ACE) for psoriasis were verified in HaCaT cells (as an immortalized human keratinocyte cell line) and imiquimod (IMQ)‐induced psoriasis‐like mouse models. In HaCaT cells, IC₅₀ value of ACE was 37.5 μg/ml after incubating for 72 hr. The antiproliferation activity of ACE in HaCaT cells was further verified by apoptosis assays. The percentage of apoptotic population in ACE‐treated group was significantly higher than that of control group (p < .05). The result of cell cycle arrest assay also supported the observed antiproliferation efficacy of ACE in HaCaT cells. In IMQ‐induced psoriasis‐like mouse models, the Psoriasis Area and Severity Index score of ACE (50 mg/ml; ACE50)‐treated group was significantly lower than that of IMQ group on Day 4 (p < .05). After topical application of ACE on psoriasis‐like lesion for 4 days, the epidermal thickness of (IMQ + ACE50) group was significantly lower than that of IMQ group (p < .05). The expression levels of Ki‐67 and intracellular adhesion molecule‐1 in excised skin tissues of (IMQ + ACE50) group were also lower than those of IMQ group. All these findings suggest that ACE can be used as a promising antipsoriatic agent.     

核桃青皮流浸膏对银屑病小鼠皮肤屏障功能的影响及机制研究

目的探讨核桃青皮流浸膏对咪喹莫特乳膏致银屑病小鼠皮肤屏障功能的影响及机制。方法制备不同浓度的核桃青皮流浸膏,采用咪喹莫特乳膏制作银屑病模型,给药后通过PASI评分、HE染色观察各组小鼠皮肤变化及组织结构变化,利用RT-PCR检测各组小鼠皮肤组织中水通道蛋白-3(aquaporin3,AQP3)、神经酰胺(ceramide,Cer),丝聚合蛋白(filaggrin,FLG)、含半胱氨酸的天冬氨酸蛋白水解酶-14(Caspase14)四种相关保湿因子表达的改变。结果给予不同浓度核桃青皮流浸膏的实验组较模型组皮损部位红肿程度轻、鳞屑面积小,皮肤光滑,增厚程度轻,镜下表皮增生情况有缓解,尤其高剂量组较假手术组无显著性差异(P>0.01);中、高剂量组AQP3、Cer、FLG、Caspase14表达分别与模型组比较均具有显著性差异(P<0.01),高剂量与阳性药组相比,四种物质的表达均不具有显著性差异(P>0.01)。结论核桃青皮流浸膏对咪喹莫特乳膏致银屑病小鼠模型病理的变化有改善作用,其增强皮损组织中AQP3、Cer、FLG、Caspase14四种相关保湿因子的表达是改善皮肤损伤的可能机制之一,治疗作用与给药量成线性关系,且高浓度效果不劣于卡泊三醇组。     

基于Notch信号通路探讨银屑平丸对银屑病模型小鼠皮损及血清炎性因子的调节作用

目的:探究银屑平丸通过调控Notch信号通路对银屑病(PS)小鼠模型皮损及血清炎性因子的调节作用,进一步探讨银屑平丸对PS的治疗机制。方法:将50只BALB/c小鼠按照完全随机原则分为空白对照组、模型组、阿维A胶囊组、银屑平丸组、阿维A胶囊加银屑平丸组(联合用药组)等五组,每组10只。以5%咪喹莫特乳膏涂抹小鼠背部暴露皮肤进行造模,抹药的同时以药物进行干预。实验过程中每日记录各组小鼠的皮损变化,末次给药24 h后,观察每组小鼠皮损变化并予以PS皮损面积及严重程度指数(PASI)评分,酶联免疫吸附测定(ELISA)法检测各组小鼠血清白细胞介素-32(IL-32)、白细胞介素-33(IL-33)、白细胞介素-36(IL-36)等炎性因子的表达水平,Western blot检测皮损组织中Notch受体1(Notch1)、JAGGED1蛋白(Jagged-1)、Hes1转录因子(Hes-1)等蛋白水平的表达。实时定量PCR检测皮损组织中Notch1、Jagged-1、Hes-1等的mRNA的表达。结果:与空白对照组相对比,模型组、阿维A胶囊组、银屑平丸组、联合用药组小鼠背部皮损的严重程度通过计算PASI评分均有显著升高(P<0.05); 与模型组相对比,阿维A胶囊组、银屑平丸组、联合用药组小鼠背部皮损的严重程度通过计算PASI评分均有显著降低(P<0.05),其中联合用药组效果最佳(P<0.05); HE染色结果亦证实联合用药组的病理缓解程度最佳(P<0.05); ELISA结果显示,阿维A胶囊组、银屑平丸组、联合用药组均可显著降低小鼠血清IL-32、IL-33、IL-36水平,其中联合用药组效果最佳(P<0.05); Western blot及RT-PCR结果显示,阿维A胶囊组、银屑平丸组、联合用药组均可显著降低小鼠皮损组织的Notch1、Jagged-1、Hes-1蛋白表达及mRNA表达,且联合用药组效果最优(P<0.05)。结论:银屑平丸能有效改善PS小鼠模型的皮损情况,同时与阿维A胶囊联合使用起到协同增效作用,其作用机制可能与银屑平丸能够抑制Notch信号通路相关蛋白表达相关。     

养血解毒方对银屑病角质形成细胞紧密连接的调节作用

目的:观察银屑病样小鼠皮损紧密连接蛋白中水闸蛋白(claduin-1,claudin-7),闭锁蛋白(occludin)的表达,明确养血解毒方对银屑病表皮通透屏障的修复作用,为养血解毒方治疗银屑病提供科学依据。方法:将C57BL/6J小鼠随机分为空白组、模型组、甲氨喋呤组、养血解毒方组,制备甲氨喋呤溶液、养血解毒方水煎剂对应灌胃干预,同时小鼠背部剃毛后给予咪喹莫特涂抹诱导银屑病样皮损模型。每日拍照记录皮损形态并对严重程度指数(PASI)评分;水油测试笔检测皮损表皮含水量;苏木素-伊红(HE)染色观察其病理改变、测量表皮厚度;免疫荧光法检测增殖相关的核抗原(Ki67);免疫组化法检测表皮兜甲蛋白(loricrin),真皮中CD3^+T淋巴细胞浸润和紧密连接蛋白claduin-1,claudin-7,occludin的表达;蛋白免疫印迹法(Western blot)检测皮损中claudin-7,occludin的表达。模拟银屑病皮损微环境,建立白细胞介素-17(IL-17,1 mg·L^-1)刺激的角质形成细胞(Hacat)模型,制作养血组分、解毒组分、养血解毒方喷干粉进行干预。采用细胞增殖毒性检测试剂盒-8(CCK-8)法检测药物对Hacat细胞的毒性;细胞免疫荧光法检测药物对角质形成细胞claudin-1,claudin-7,occludin表达的干预作用。结果:与模型组比较,养血解毒方可显著减轻小鼠银屑病样皮损表现,降低PASI评分及皮损表皮厚度(P<0.01),增加皮损区表皮水分含量(P<0.01),减少表皮ki67,loricrin的异常表达和真皮CD3+T细胞浸润(P<0.01),并增加紧密连接蛋白claudin-1,claudin-7,occludin的表达(P<0.05),增加紧密连接结构的完整性;体外研究发现,与模型组比较,养血解毒方组和养血组分组明显升高紧密连接蛋白claudin-1,claudin-7,occludin的表达(P<0.05);与模型组比较,解毒组分组蛋白表达水平无统计学差异。结论:养血解毒方通过调节角质形成细胞间紧密连接的表达抑制其异常的增殖分化过程,进一步恢复破坏的表皮通透屏障,可能是其治疗银屑病的作用机制之一。其中养血解毒方的养血组分对调节紧密连接的修复起主要作用。     

黄芍银屑颗粒对银屑病样动物模型的影响

目的:研究黄芍银屑颗粒是否有治疗银屑病的作用。方法:选取3.125、6.25、12.5、25 g生药/kg黄芍银屑颗粒的药物剂量,经口灌胃连续给药1或2周。研究黄芍银屑颗粒对小鼠阴道上皮细胞、小鼠尾部鳞片表皮颗粒层形成、小鼠血清CD3、CD4和CD8影响以及对心得安所致豚鼠耳廓皮损的影响。结果:黄芍银屑颗粒有明显抑制小鼠阴道上皮细胞有丝分裂,并可明显促进小鼠尾部鳞片表皮颗粒层的形成,具有降低小鼠血清CD4和CD8比值的趋势,从而可能调节动物的异常免疫反应,对心得安所致豚鼠耳廓皮损有明显的治疗作用。结论:黄芍银屑颗粒有治疗银屑病的作用。     

走罐疗法治疗血瘀证斑块状银屑病皮损表皮增生的临床观察

目的:观察走罐疗法对血瘀证斑块状银屑病皮损表皮厚度的影响。方法:收集2019年1月至2020年3月就诊于新疆医科大学附属中医医院皮肤科门诊及住院的80例血瘀证斑块状银屑病患者,随机分为治疗组与对照组,每组40例。治疗组采用走罐疗法,对照组采用NB-UVB治疗,共治疗4周。观察两组患者治疗前后银屑病PASI评分变化,并利用反射式共聚焦显微镜(RCM)分别检测两组患者皮损表皮厚度的变化。结果:两组治疗后PASI评分、皮损表皮厚度均显著优于治疗前(P<0.01),且治疗组PASI差值、皮损表皮厚度差值显著优于对照组(P<0.01,P<0.05)。治疗组总有效率为85.0%(34/40),显著优于对照组总有效率50.0%(20/40)(P<0.01)。结论:走罐疗法对血瘀证斑块状银屑病表皮增生的改善优于NB-UVB的治疗。     

补肾益精法中药复方对硬皮病小鼠皮肤纤维化的影响

目的:研究补肾益精法中药复方对硬皮病小鼠皮肤纤维化表型的影响。方法:使用博来霉素诱导建立硬皮病小鼠模型,分别采用补肾益精法中药复方(中药复方组)、生理盐水(模型组)处理硬皮病模型小鼠,共3周,并设正常对照组。HE染色观察皮肤病理改变;使用实时定量逆转录-聚合酶链反应(RT-PCR)技术,测定各组小鼠I型胶原α2(COLⅠα2)基因表达情况。结果:成功建立硬皮病小鼠模型,皮肤病理HE染色显示,中药复方组小鼠皮肤纤维化有不同程度改善。模型组小鼠COLⅠα2基因表达较正常对照组高(P<0.01);经补肾益精法处理后,中药复方组小鼠COLⅠα2基因表达减少,与正常对照组比较,差异无显著性意义(P>0.05)。结论:补肾益精法中药复方可改善硬皮病模型小鼠皮肤纤维化程度。