Expression of Bcl-2, Bax and Caspase-3 in Nerve Tissues of Rats Chronically Exposed to 2,5-hexanedione

Authors: Cui, Ning; Li, Shanxia; Zhao, Xiulan; Zhang, Tianliang; Zhang, Cuili; Yu, Lihua; Zhu, Zhengping; Xie, Keqin

Source: Neurochemical Research, Volume 32, Number 9, September 2007 , pp. 1566-1572(7)

Publisher: Springer

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Abstract:

Occupational exposure and experimental intoxication with n-hexane or its metabolite 2,5-hexanedione (HD) produce a central-peripheral neuropathy. However, the mechanism remains unknown. We hypothesized that HD affected the expression of Bcl-2, Bax and Caspase-3 in the central nervous system (CNS) and the peripheral nervous system (PNS). Male adult Wistar rats were administered by intraperitoneal injection at a dosage of 200 or 400 mg/kg HD, five days per week for 8 weeks. Samples of the cerebral cortex, cerebellum, spinal cord and sciatic nerves were collected and examined for Bcl-2, Bax and Caspase-3 expression using Western blotting. Subchronic exposure to HD resulted in significantly increased expression of both anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax and Caspase-3 in cerebral cortex and cerebellum, which exhibited a dose-dependent pattern. Though little change was detected in spinal cord, our results showed that the expression of Bcl-2, Bax and Caspase-3 was markedly enhanced in the sciatic nerves. These findings suggested that the changes of apoptosis-related protein level in rat nerve tissues were associated with the intoxication of HD, which might be involved in early molecular regulatory mechanism of apoptosis in the HD-induced neuropathy.

Keywords: 2,5-hexanedione; Nerve tissue; Apoptosis; Bcl-2; Bax; Caspase-3

Document Type: Research article

DOI: http://dx.doi.org/10.1007/s11064-007-9359-0

Affiliations: 1: Email: keqinx@sdu.edu.cn

Publication date: 2007-09-01