文章摘要
汪一晗,邢凤玲,傅宏阳,等.发物对接触性皮炎模型大鼠的影响[J].浙江中医药大学学报,2021,(3):222-228.
发物对接触性皮炎模型大鼠的影响
The Effect of Stimulating Food on Contact Dermatitis Model Rats
投稿时间:2020-05-20  
DOI:10.16466/j.issn1005-5509.2021.03.003
中文关键词: 接触性皮炎  发物  牛肉  羊肉  胃肠湿热  炎症因子  发病机制  Notch1
英文关键词: contact dermatitis  stimulating food  beef  mutton  gastrointestinal dampness-heat  inflammatory cytokine  pathogenesis  Notch1
基金项目:浙江省中医药(中西医结合)重点学科建设项目(2Z11912)
作者单位E-mail
汪一晗 浙江中医药大学第一临床医学院 杭州 310053  
邢凤玲 浙江中医药大学第一临床医学院 杭州 310053  
傅宏阳 浙江中医药大学第一临床医学院 杭州 310053  
岑璐莎 浙江省中医院  
杨晓红 浙江省中医院  
曹毅 浙江省中医院 caoyi1965@163.com 
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中文摘要:
      [目的]观察传统发物牛羊肉对接触性皮炎(contact dermatitis,CD)模型大鼠的影响。[方法]25只无特定病原体(specific pathogen free,SPF)级雄性SD大鼠随机分为牛肉组、羊肉组、胃肠湿热组、模型对照组、空白组,每组5只。牛肉组、羊肉组、胃肠湿热组、模型对照组用脱毛膏诱导CD模型,其中牛肉组、羊肉组、胃肠湿热组大鼠以肥甘饮食构造胃肠湿热模型,从造模前1d开始,牛肉组与羊肉组改用含牛肉或羊肉的肥甘饲料饲喂3d,直至造模成功48h后取材,饲喂次数及剂量等同于正常进食。诱发成功时及诱发48h后观察大鼠皮损表现。苏木精-伊红(hematoxylin-eosin,HE)染色法观察大鼠皮肤病理变化,酶联免疫吸附检测(enzyme linked immunosorbent assay,ELISA)法检测血清白细胞介素-35(interleukin-35,IL-35)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)水平,免疫组化检测大鼠皮肤及消化道组织中Notch1蛋白的表达并进行定性评估。[结果]脱毛膏诱导后大鼠出现红斑、水肿等急性CD样表现,且牛肉组、羊肉组中大鼠皮损明显严重于胃肠湿热组和模型对照组。病理结果提示,除空白组外,各组均出现细胞间水肿及炎症细胞浸润的表现,且牛肉组、羊肉组和胃肠湿热组明显严重于模型对照组。Notch1在胃肠道和皮肤的表达,牛肉组、羊肉组均为强阳性;胃肠湿热组均为阳性;模型对照组在皮肤组织中呈弱阳性,胃肠道中呈阴性;空白组均为阴性。牛肉组、羊肉组TNF-α水平明显高于模型对照组(P<0.05);牛肉组IL-35水平明显低于模型对照组(P<0.05),羊肉组与模型对照组差异无统计学意义(P>0.05)。[结论]发物牛羊肉能加重CD症状,并可能与上调胃肠道Notch1表达和血清中TNF-α水平、下调IL-35水平有关。
英文摘要:
      [Objective]To observe the effect of traditional stimulating food, beef and mutton, on contact dermatitis(CD) model rats. [Methods]Twenty-five specific pathogen free(SPF) male SD rats were randomly and equally divided into 5 groups: Beef group, mutton group, gastrointestinal dampness-heat group, model control group and blank group. The CD model was induced by depilatory cream in beef group, mutton group, gastrointestinal dampness-heat group and model control group. The rats in beef group, mutton group and gastrointestinal dampness-heat group were fed with fat diet to construct gastrointestinal dampness-heat model. After that, beef group and mutton group were fed with fat diet containing beef or mutton for 3 days until 48 hours after successful modeling. The feeding time and doses were equal to normal feeding.The skin lesions of the rats were observed at the time of successful induction and 48h later. After 48h, hematoxylin-eosin(HE) staining was used to observe the pathological changes of rat skin, serum interleukin-35(IL-35) and tumor necrosis factor-α(TNF-α) levels were detected by enzyme linked immunosorbent assay(ELISA), and the expression of Notch1 protein in rat skin and digestive tract tissues was detected by immunohistochemistry, and evaluated and compared by scoring. [Results]Erythema, edema and other lesions of acute CD were observed in the rats induced by depilatory cream, and the skin lesions of the rats in beef group and mutton group were more serious than those in gastrointestinal dampness-heat group and model control group. The pathological results indicated that, except blank group, there were signs of intercellular edema and inflammatory cell infiltration in each group, and beef group, mutton group and gastrointestinal dampness-heat group were significantly more severe than model control group. The expression of Notch1 in gastrointestinal tract and skin was strongly positive in beef group and mutton group. The expression in gastrointestinal tract and skin in dampness-heat group was all positive; in model control group, the expression was weakly positive in the skin tissue and negative in the gastrointestinal tract. The expression in all tissue in blank group was negative.The serum level of TNF-α in beef group and mutton group was significantly higher than that of model control group(P<0.05). The serum level of IL-35 in beef group was significantly lower than that in model control group(P<0.05), and there was no significant difference between mutton group and model control group(P>0.05). [Conclusion]The stimulating food beef and mutton can aggravate symptoms of CD, which may be related to the upregulation of expression of gastrointestinal Notch1 and serum level of TNF-α, and the downregulation of level of IL-35.
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