论文部分内容阅读
目的建立以低硒饲料、T-2毒素染毒大鼠大骨节病(KBD)动物模型,检测低硒及T-2毒素对各组大鼠血清中白介素-6(IL-6)、白介素-1β(IL-1β)及肿瘤死亡因子-α(TNF-α)水平的影响,探讨这些细胞因子在KBD发病机制中的作用。方法断乳SD大鼠随机分为常规组和低硒组2组饲养一个月,确定大鼠处于低硒状态后,再将大鼠随机分为6组,T-2毒素灌胃饲养一个月后处死,依实验设计留取大鼠血清,采用酶联免疫吸附测定(ELISA)技术检测IL-6、IL-1β和TNF-α的水平。结果低硒或高/低T-2干预各组大鼠血清IL-6、IL-1β、TNF-α浓度水平与常规组相比均有显著性升高,低硒和T-2毒素干预各组大鼠血清IL-6浓度水平与常规组比较增高3～5倍,IL-1β和TNF-α浓度水平与常规组比较也增高1～2倍,且与常规组相比有显著性差异(P<0.05);IL-6、IL-1β、TNF-α的水平常规加低T-2组与低硒组比较没有显著性差异(P>0.05);常规加高/低T-2组2组比较没有显著性差异(P>0.05),低硒加高/低T-2 2组相比有显著性差异(P<0.01),低硒加高/低T-2 2组与其他干预组比较均有显著性差异(P<0.01)。结论细胞因子IL-6、IL-1β和TNF-α在KBD发病、发展中起着重要作用,在低硒条件下,高T-2毒素的毒性作用更强,低硒是IL-1β、IL-6和TNF-α浓度升高的重要条件,病情严重程度与T-2毒素存在剂量依赖关系。在常规加高/低T-2组,硒有一定的保护作用但并不能抑制T-2毒素对病情发展的作用。本结果为低硒条件下T-2毒素在KBD病因中的作用提供了实验依据。
Objective To establish a rat model of KBD induced by low-selenium diet and T-2 toxin, and to detect the effect of low selenium and T-2 toxin on interleukin-6 (IL-6), interleukin- 1β (IL-1β) and tumor necrosis factor-α (TNF-α), and to explore the role of these cytokines in the pathogenesis of KBD. Methods Weaning SD rats were randomly divided into routine group and low selenium group 2 feeding one month to determine the rats in a low selenium state, and then the rats were randomly divided into 6 groups, T-2 toxin feeding one month after gavage The rats were sacrificed and the serum of rats was collected according to the experimental design. The levels of IL-6, IL-1β and TNF-α were detected by enzyme linked immunosorbent assay (ELISA). Results The levels of IL-6, IL-1β and TNF-α in sera of rats with low selenium or high / low T-2 intervention significantly increased compared with the control group, and the intervention of low selenium and T-2 toxin Compared with the conventional group, the level of IL-6 in serum increased 3 ~ 5 times and the level of IL-1β and TNF-α increased 1 ~ 2 times compared with the conventional group, and there was significant difference compared with the conventional group (P <0.05). There was no significant difference in the levels of IL-6, IL-1β and TNF-α between normal low T-2 group and low-selenium group (P> 0.05) There was no significant difference between the low selenium group (P> 0.05), low selenium increased group / low T-2 2 group (P <0.01), low selenium increased / low T-2 2 group and other intervention groups There were significant differences (P <0.01). Conclusions The cytokines IL-6, IL-1β and TNF-α play an important role in the pathogenesis and development of KBD. Under the condition of low selenium, T-2 toxin is more toxic and selenium is IL-1β, IL -6 and TNF-α levels of the important conditions, the severity of the disease and T-2 toxin in a dose-dependent manner. In conventional elevated / low T-2 group, selenium has a protective effect but does not inhibit the T-2 toxin on the progression of the disease. The results provide an experimental basis for the role of T-2 toxin in KBD under low selenium conditions.