Abstract
This study was to explore the mechanisms underlying 1,2-dichloroethane (1,2-DCE) induced brain edema by focusing on alteration of matrix metalloproteinase-2 (MMP-2) in rat astrocytes induced by 2-chloroethanol (2-CE), an intermediate metabolite of 1,2-DCE in vivo. Protein and mRNA levels of MMP-2, and the phosphorylated protein levels of p38 MAPK (p-p38), extracellular signal regulated protein kinase (p-ERK1/2) and c-Jun N-terminal kinase (p-JNK1/2) in astrocytes were examined by immunostaining, western blot or real-time RT-PCR analysis. Findings from this study disclosed that protein levels of MMP-2 were upregulated by 2-CE in astrocytes. Meanwhile, protein levels of p-p38, p-ERK1/2 and p-JNK1/2 were also increased apparently in the cells treated with 2-CE. Moreover, pretreatment of astrocytes with SB202190 (inhibitor of p38 MAPK), U0126 (inhibitor of ERK1/2) or SP600125 (inhibitor of JNK1/2) could suppress the upregulated expression of p-p38, p-ERK1/2, and p-JNK1/2. In response to suppressed protein levels of p-p38 and p-JNK1/2, the protein levels of MMP-2 also decreased significantly, indicating that activation of MAPK signal pathways were involved in the mechanisms underlying 2-CE-induced upregulation of MMP-2 expression.
Highlights
The compound of 1,2-dichloroethane (1,2-DCE, CAS number: 107-06-2) is one of the most widely produced halocarbons, and used mainly in the production of vinyl chloride worldwide
Expressions of matrix metalloproteinase-2 (MMP-2) in Astrocytes Affected by 2-CE Treatment
Results of present study suggested that the protein levels of MMP2 in rat astrocytes could be upregulated by 2-CE treatment
Summary
The compound of 1,2-dichloroethane (1,2-DCE, CAS number: 107-06-2) is one of the most widely produced halocarbons, and used mainly in the production of vinyl chloride worldwide This chemical is used as the general organic solvent, especially as the thinner of adhesives in some countries. 2-CE and chloroacetaldehyde are the reactive intermediates, and assumed to be involved in mechanisms underlying 1,2-DCE induced brain edema since they are more reactive than their parent compound (Guengerich et al, 1980; Igwe et al, 1986; Raucy et al, 1993). It is essential for exploring the neurotoxic effects induced directly by 2-CE
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