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阿的平保护纹状体神经元免受热处理损伤作用的研究 被引量:7

PROTECTIVE EFFECT OF QUINACRINE ON STRIATUM NEURONS FROM HEAT TREATMENT INJURY
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摘要 目的探讨预先使用阿的平对热处理所致的纹状体神经元损伤的保护作用及其机制,为热环境致细胞损伤的干预和药物研究提供参考。方法采用培养的大鼠纹状体神经元,培养液中加入不同浓度的阿的平,给予43℃热处理1h。台盼蓝染色鉴定细胞坏死,活性Caspase3免疫染色和原位末端转移酶法评价细胞凋亡。结果热处理明显影响神经元存活,导致细胞死亡,其中主要由细胞坏死过程介导;单独的阿的平对细胞毒性作用较小,预先使用阿的平能够减少热处理引起的细胞坏死。结论阿的平对热环境致纹状体神经元的损伤有保护作用,这种保护作用主要通过减少细胞坏死过程介导。 Aim: To study the protective effect of Quinacrine(QA) on rat striatum neurons from the injury caused by heat environment treatment, to probe the relationship between cell membrane injury and cellular injury protection, and to seek the possibility of QA as a preventive agent to heat injury. Methods: Primary cultured striatum neurons from newborn rats were pretreated with QA at diffe rent concentration for 1 h, and then heat treated at 43℃ for another 1 h. Cell necrosis was detected by Trypan blue staining, and apoptosis was evaluated through Activated Caspase 3 dye and TdT dye. Results: Heat treatment effected the survival of striatum neurons and resulted in great number of cell death, which was mainly mediated by cell necrosis process. It was shown that treatment of QA itself had little effect on the survival of striatum neurons, while QA pretreatment decreased cellular necrosis caused by following heat treatment. Conclusion: QA protects striatum neurons from heat environment injury at about 20 μmol/L, and the protection may mediated by reduction of necrosis.
出处 《中国应用生理学杂志》 CAS CSCD 北大核心 2004年第4期319-323,共5页 Chinese Journal of Applied Physiology
基金 总后勤部重点课题基金资助项目(01L024)
关键词 阿的平 热处理 细胞坏死 细胞凋亡 保护作用 Quinacrine heat treatment necrosis apoptosis protection
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  • 1Reid M S, Ho L B, Hsu K, et al, Evidence for the involvement of cyclooxygenase activity in the development of cocaine sensitization [J ]. Pharmacol Biochem Behav,2002, 71(1-2): 37-54.
  • 2Ding A S, Wang F Z. The growth characteristics of newborn rat hippocampal neurons in serum-free media [J]. Chin J Cell Biol, 1993, 15(3) :88-90.
  • 3Ronco A M, Moraga P F, Llanos M N, et al. Arachidonic acid release from rat Leydig cells: the involvement of G protein, phospholipase A2 and regulation of cAMP production[J]. J Endocrinol, 2002, 172(1): 95-104.

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