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目的研究三氯乙烯致敏小鼠体内激肽释放酶-激肽系统(KKS)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130只雌性6~8周BALB/c小鼠随机分成空白对照组、溶剂对照组、TCE处理组和TCE+PKSI-527处理组;TCE+PKSI-527处理组在17 d和19 d两次激发前24 h腹腔内注射抑制剂PKSI-527;分别于末次激发后24 h、48 h、72 h和7 d处死动物,造模期间实时记录小鼠体重,计算脏器系数,ELISA法检测血浆前激肽释放酶(PK)、高分子量激肽原(HMWK)和缓激肽(BK)水平。结果 TCE处理组的致敏率为40%,以PKSI-527干预后的致敏率为21.67%,TCE致敏组及TCE+PKSI-527组体重与空白对照组相比均明显减少;TCE处理组小鼠48 h、72 h的肝脏系数明显高于空白对照组,而使用PKSI-527干预后小鼠肾脏系数和脾脏系数均有好转。TCE处理组48 h、72 h时致敏小鼠血浆中PK浓度明显高于溶剂对照组及相应的未致敏组,且在72 h时点达到峰值,使用PKSI-527能够显著降低PK浓度。TCE处理组24 h、48 h致敏小鼠血浆中HMWK浓度明显高于溶剂对照组及相应的未致敏组;TCE+PKSI-527处理组48 h时HMWK浓度明显低于相应时段TCE致敏组。血浆BK的变化特点基本与PK和HMWK表达一致。结论 KKS活化可能参与TCE小鼠致敏及脏器免疫损伤过程。
Objective To study the expression of kallikrein-kinin system (KKS) in mice induced by trichlorethylene and to explore the pathogenesis of occupational trichlorethylene-like dermatitis (ODMLT). Methods 130 female BALB / c mice aged 6 to 8 weeks were randomly divided into blank control group, solvent control group, TCE treatment group and TCE + PKSI-527 treatment group. TCE + PKSI-527 treatment group on day 17 and 19 Animals were killed 24 h, 48 h, 72 h and 7 d after the last challenge, respectively. The body weight of mice was recorded in real time and the organ coefficient was calculated. ELISA was used to detect the expression of PKSI- Plasma kallikrein (PK), high molecular weight kininogen (HMWK) and bradykinin (BK) levels. Results The sensitization rate was 40% in TCE group and 21.67% in PKC-527 group. The body weight of TCE-sensitized group and TCE + PKSI-527 group were significantly decreased compared with the control group. TCE treatment The liver coefficient of mice at 48 h and 72 h was significantly higher than that of the blank control group, but the mice kidney index and spleen coefficient improved after PKSI-527 intervention. The concentration of PK in plasma of TCE-treated mice at 48 h and 72 h was significantly higher than that in solvent-control group and the corresponding non-sensitized group, and peaked at 72 h. The PK concentration was significantly reduced by PKSI-527. The concentration of HMWK in plasma of TCE-treated mice at 24h and 48h was significantly higher than that of solvent-control and corresponding non-sensitized mice. The concentration of HMWK in TCE + PKSI-527-treated mice was significantly lower than that of TCE at 48h group. Changes in plasma BK basically the same with the expression of PK and HMWK. Conclusion KKS activation may be involved in sensitization and organ injury in TCE mice.