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目的初步探讨大鼠大脑皮层细胞凋亡在2,5-己二酮(HD)致大鼠神经退行性病变中的作用。方法 60只Wistar雄性大鼠,经腹腔染毒,剂量分别为100和300 mg/(kg·d),连续8周(每周5 d)。处死一半动物并分离、冻存大脑组织。另一半动物停止染毒、自然恢复8周后取材。采用TUNEL方法检测大鼠大脑皮层细胞凋亡指数(AI),采用免疫组化方法检测大鼠大脑皮层细胞Bcl-2和Bax的相对含量。结果染毒8周后,100和300 mg/kg剂量组动物AI分别为22.25%(P<0.05)和25.12%(P<0.05),与对照组7.94%比较,阳性细胞数量明显增加。恢复8周后100和300 mg/kg剂量组动物AI分别为18.45%(P<0.05)和17.20%(P<0.05),与对照组7.48%比较,仍存在显著性差异,但300 mg/kg剂量组动物AI较染毒8周时有所减小;100和300 mg/kg剂量组动物在HD染毒8周和8周+恢复8周时,Bcl-2含量分别相当于对照组的89.2%、78.4%和80.9%、132.9%;Bax含量分别相当于对照组的126.3%、135.6%和74.6%、80.9%。结论 HD致大鼠退行性病变过程中可能伴有大脑皮层细胞凋亡的发生。
Objective To investigate the role of apoptosis of rat cerebral cortex in neurodegenerative diseases induced by 2,5-hexanedione (HD) in rats. Methods Sixty male Wistar rats were treated intraperitoneally with doses of 100 and 300 mg / (kg · d) for 8 weeks (5 days a week). Half of the animals were sacrificed and isolated, frozen in brain tissue. The other half of the animals stopped exposure and recovered naturally after 8 weeks. The apoptosis index (AI) of rat cerebral cortex was detected by TUNEL method. The relative content of Bcl-2 and Bax in rat cerebral cortex cells was detected by immunohistochemistry. Results After 8 weeks of exposure, AI in the 100 and 300 mg / kg groups were 22.25% (P <0.05) and 25.12% (P <0.05), respectively. Compared with 7.94% in the control group, the number of positive cells increased significantly. After 8 weeks of resuscitation, the AI of animals in the 100 and 300 mg / kg groups were 18.45% (P <0.05) and 17.20% (P <0.05), respectively, but there was still significant difference compared with the control group of 7.48% Compared with the control group, the levels of Bcl-2 in the animals treated with 100 and 300 mg / kg HD for 8 weeks and 8 weeks and 8 weeks after recovery were respectively 89.2% %, 78.4% and 80.9%, 132.9%, respectively; Bax content was equivalent to 126.3%, 135.6% and 74.6% and 80.9% of the control group respectively. Conclusion HD-induced rat degeneration may be associated with cerebral cortical apoptosis.