Impact of Sub-chronic Aluminium-maltolate Exposure on Catabolism of Amyloid Precursor Protein in Rats

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• 作者：Rui Feng LIANG ; Wei Qing LI ; Hong WANG ; Jun Xia WANG ; Qiao NIU
• 关键词：Aluminium-maltolate ; Amyloid precursor protein ; ¦Â-amyloid protein ; Rat
• 刊名：Biomedical and Environmental Sciences
• 出版年：2013
• 出版时间：June, 2013
• 年：2013
• 卷：26
• 期：6
• 页码：445-452
• 全文大小：1553 K

文摘

Objective

To investigate the impact of sub-chronic Aluminium-maltolate [Al(mal)₃] exposure on the catabolism of amyloid precursor protein (APP) in rats.

Methods

Forty adult male Sprague-Dawley (SD) rats were randomly divided into five groups: the control group, the maltolate group (7.56 mg/kg BW), and the Al(mal)₃ groups (0.27, 0.54, and 1.08 mg/kg BW, respectively). Control rats were administered with 0.9 % normal saline through intraperitoneal (i.p.) injection. Maltolate and Al(mal)₃ were administered to the rats also through i.p. injections. Administration was conducted daily for two months. Rat neural behavior was examined using open field tests (OFT). And the protein expressions and their mRNAs transcription related with APP catabolism were studied using enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR).

Results

The expressions of APP, ¦Â-site APP cleaving enzyme 1 (BACE1) and presenilin-1 (PS1) proteins and their mRNAs transcription increased gradually with the increase of Al(mal)₃ doses (P<0.05). The enzyme activity of BACE1 in the 0.54 and 1.08 mg/kg Al(mal)₃ groups increased significantly (P<0.05). The expression of ¦Â-amyloid protein (A¦Â) 1-40 gradually decreased while the protein expression of A¦Â1-42 increased gradually with the increase of Al(mal)₃ doses (P<0.05).

Conclusion

Result from our study suggested that one of the possible mechanisms that Al(mal)₃ can cause neurotoxicity is that Al(mal)₃ can increase the generation of A¦Â1-42 by facilitating the expressions of APP, ¦Â-, and ¦Ã-secretase.