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目的探讨异佛尔酮二异氰酸酯(IPDI)对大鼠肝、肺的氧化损伤作用,研究其对体液免疫的影响及其可能机制,为后续研究提供实验依据。方法选择健康SPF级Wistar雄性大鼠80只,随机分为高剂量(1/4LD50)、中剂量(1/8LD50)、低剂量(1/16LD50)组和溶剂对照组(玉米油),每组20只,采用腹腔注射IPDI的方式进行染毒,连续染毒13周,每天1次。于末次染毒后24 h,对清醒状态下的实验动物进行眼眶静脉采血,测定血清中免疫球蛋白Ig G、Ig A、Ig M、Ig E和补体C3、C4的含量。然后将全部实验动物断头处死,测定肝脏、肺脏组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)的活力以及丙二醛(MDA)的含量。结果高、中剂量组大鼠肝脏SOD、CAT、GSH-Px活力均明显低于对照组(均P<0.01);高、中剂量组大鼠肝脏MDA含量明显高于对照组(均P<0.01)。高、中、低剂量组大鼠肺脏SOD、GSH-Px活力和高、中剂量组CAT活力均明显低于对照组(均P<0.01);高、中剂量组大鼠肺脏MDA含量均明显高于对照组(均P<0.01)。高剂量组大鼠血清Ig G、Ig M含量和高、中剂量组Ig A、C3含量均明显低于对照组(均P<0.01)。结论 IPDI可产生氧自由基,引起肝脏、肺脏组织的氧化损伤,并可导致免疫球蛋白Ig G、Ig A、Ig M和补体C3水平下降,抑制大鼠体液免疫,但其机制仍需进一步研究。
Objective To investigate the effects of isophorone diisocyanate (IPDI) on the oxidative damage of liver and lung in rats, and to study the effect of IPDI on humoral immunity and its possible mechanism, so as to provide experimental basis for the follow-up study. Methods Eighty healthy Wistar male SPF rats were randomly divided into high dose (1 / 4LD50), medium dose (1/8 LD50), low dose (1/16 LD50) and solvent control group (corn oil) Twenty mice were injected intraperitoneally with IPDI for 13 weeks and once daily. At 24 h after the last exposure, orbital venous blood was collected from the experimental animals under awake condition, and the contents of immunoglobulin Ig G, Ig A, Ig M, Ig E and complement C3 and C4 in serum were measured. All animals were then sacrificed by decapitation to determine the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in the liver and lung tissues, (MDA) content. Results The activities of SOD, CAT and GSH-Px in liver of rats in high and middle dose groups were significantly lower than those in control group (all P <0.01). The contents of MDA in liver of high and middle dose groups were significantly higher than those in control group ). The activities of SOD and GSH-Px in the lungs of high, middle and low dose groups were significantly lower than those in the control group (all P <0.01). The MDA content in the lungs of high and middle dose groups was significantly higher In the control group (all P <0.01). The contents of Ig G and Ig M in high-dose and high-dose and middle-dose groups were significantly lower than those in control group (all P <0.01). Conclusions IPDI can produce oxygen free radicals and cause oxidative damage in the liver and lung tissues. IPDI can reduce the immunoglobulin Ig G, Ig A, Ig M and complement C3 levels and inhibit humoral immunity in rats, but the mechanism remains to be further studied .