中文摘要：

目的研究三氯乙烯（TCE）致敏小鼠肾脏免疫损伤过程中缓激肽及其受体B1R和B2R的表达水平，探讨职业性三氯乙烯药疹样皮炎（ODMLT）的发病机制。方法将6-8周雌性BALB／c小鼠随机分成空白对照组（5只）、溶剂对照组（5只）、TCE处理组（60只）和PKSI-527＋TCE处理组（60只），于动物处理的第1、4、7、10天进行致敏，第17、19天进行激发，且PKSI-527＋TCE处理组在每次激发前24h进行腹腔内注射抑制剂PKSI-527（50mg／kg），末次激发后24、48、72h和7d处死动物，记录体重和肾脏重量，无菌取血液及肾脏组织，用ELISA法检测血浆BK水平并对肾脏做病理观察，用免疫荧光法检测肾脏组织BIR和B2R表达水平。结果TCE处理组中的致敏小鼠可见明显的肾脏细胞间质内的炎细胞浸润，肾小管上皮细胞空泡样变性。PKSI-527＋TCE处理组中的致敏小鼠的肾脏病理与同时点的TCE致敏组比较，损伤较之明显减轻。24、48和72hTCE处理组的致敏组小鼠血浆BK表达明显高于溶剂对照组及相应的未致敏组，且72h明显高于PKSI-527＋TCE致敏组的相应时点，差异有统计学意义（P〈0．05）。24、48、72h和7dTCE处理组的致敏小鼠B1R和B2R在肾脏中的表达水平明显高于溶剂对照组以及相应时点的未致敏组。PKSI-527＋TCE致敏组的4个时点的肾脏中B1R和B2R的表达水平都较TCE致敏组的相应时点的表达降低。结论KKS活化可能参与TCE致敏小鼠的肾脏免疫损伤过程，且BK及其受体B1R和B2R表达改变在此过程中可能发挥重要作用。

英文摘要：

Objective To study the expression of bradykinin and its receptors B1R and B2R in the kidney immune injury in trichloroethylene-sensitized mouse and discuss the pathogenesis of Dermatitis Medicamentosa-like of TCE （ODMLT）. Methods On the first days, intradermal injection by 50% TCE and the amount of FCA mixture 100μl for initial sensitization; on 4, 7, 10 days, painted abdominal skin by 100 μl 50% TCE for three sensitization, on 17, 19 days, painted on the back skin by 100 μl 30% TCE for initial excitation and the last challenge; 24 h before each challenge, PKSI-527＋TCE group received intraperitoneal injection by inhibitor PKSI-527 （50 mg/kg）; solvent control group treat without TCE and sensitization and excitation reagent the same proportion of olive oil and acetone mixture, blank control group without any treatment. Before killing the mouse, renal weight and body weight were recorded. The renals and plasma were separated at 24 h, 48 h, 72 h and 7 d after the last challenge and observed pathological of the renals. Expression of B1R and B2R in renal were examined by immunofluorescence technique. Plasma were examined by ELISA for BK. Results The renal pathological examination revealed the apparent damage of TCE sensitized mice which compared to solvent control group showed obvious cellular infiltration, vacuolar degeneration of renal tubular epithelial cells. The renal damage of PKSI-527＋TCE-sensitized groups which compared to the corresponding point of TCE-sensitized groups showed significantly reduced. The expression of BK in 24 h, 48 h and 72 h TCE-sensitized groups were significant higher than solvent control group and related TCE non-sensitized groups （P〈0.05） and 72 h point compared to the corresponding point of PKSI-527＋TCE group was also increased,, the difference was statistically significant （P〈0.05）. The expression levels of B1R and B2R in the kidney in 24 h, 48 h, 72 h and 7 d TCE- sensitized groups were obviously higher than solvent control group and related TCE non-sensiti