摘要
目的探讨PM2.5暴露对大鼠凝血功能的影响及机制。方法24只雌性SD大鼠随机分为4组:对照组、PM2.53.75mg/kg组、PM257.5mg/kg组、PM2s15mg/kg组。将大鼠暴露于不同剂量PM2.5,24h后处死大鼠,取大鼠血浆检测凝血酶原时间(PT)、活化的部分凝血活酶时间(APTT)、纤维蛋白原(FIB),取BALF显微镜下细胞计数及分类,大鼠肺脏石蜡切片HE染色观察病理改变,酶联免疫吸附试验法检测BALF中IL-6、肿瘤坏死因子α(TNFd)含量、肺组织丙二醛(MDA)含量及血清血管性血友病因子(vWF)含量,蛋白免疫电泳法(Westernblot)检测血管紧张素Ⅱ的1型受体(ATl)蛋白表达。结果PM2.57.5mg/kg组、PM2.5 15mg/kg组PT、APTT值较对照组及PM2.53.75mg/kg组缩短(P〈0.05),各组血浆FIB值均无统计学差异(P〉0.05)。PM2.5各剂量组BALF中细胞总数及中性粒细胞比例均明显高于对照组(P〈0.05),且随着PM2.5剂量增加而呈剂量依赖性升高。PM2.57.5mg/kg组和PMzs15mg/kg组BALF中II-6、TNF-α含量、肺组织MDA含量、血清vwF含量及肺组织ATl受体蛋白表达明显高于对照组及PM2.53.75mg/kg组(P〈0.05)。结论PM2.5暴露可导致PT、APTT缩短,诱发血液高凝,其机制可能与炎症反应及血管内皮损伤相关。
Objective To investigate the effect of PM2 s on coagulation in rats,and further elucidate its mechanism on inflammation and endothelial injury. Methods A total of 24 rats were divided into four groups. We developed a rat model in which the animals were exposed to PM2.5 in a 24h dose-response study (3.75 mg/kg,7.5 mg/kg,and 15 mg/kg). Prothrombintime (PT),activated partial thromboplastin time (APTT),and fibringen (FIB) in plasma were detected. The total and differential cell counts in the BALF were observed. The contents of malondialdebyde (MDA), interleukin-6 (IL-6), tumor necrosis factor-a (TNF-6), and von Willebrand factor (vWF) were detected by ELISA. Western blot was performed to detect the protein level of angiotensin H type 1 receptor (AT1). Results PT and APTT in 7.5 mg/kg group and 15 mg/kg group were obviously shortened than those in control group and 3.75 mg/kg group ( P 〈 0.05). The total cell number and the percentage of neutrophils in BALF in 3.75 mg/kg group,7.5 mg/kg group,and 15 mg/kg group were obviously higher than those in control group. The contents of MDA, IL-6, TNF u,and vWF in 7.5 mg/kg group and 15 mg/kg group were obviously higher than those in control group and 3.75 mg/kg group. And the protein level of AT1 in lung of 7.5 mg/kg group and 15 mg/kg group was obviously higher than those in control group and 3.75 mg/kg group. Conclusions PT and APTT can be shortened by short-term exposure to PM2.5 , and that would lead to hypercoagulable state,which is related to inflammatory changes and endothelial damage.
出处
《国际呼吸杂志》
2014年第22期1710-1714,共5页
International Journal of Respiration