Minocycline reduces oxygen-glucose deprivation-induced PC12 cell cytotoxicity via matrix metalloproteinase-9, integrin beta 1 and phosphorylated Akt modulation

• Published in: Neurological sciences 2013-08, Vol.34 (8), p.1391-1396
• Main Authors: Chen, Xiaohong, Chen, Shaoqiong, Jiang, Ying, Zhu, Cansheng, Wu, Aimin, Ma, Xiaomeng, Peng, Fuhua, Ma, Lili, Zhu, Dongliang, Wang, Qing, Pi, Rongbiao
• Format: Article
• Language: English
• ISSN: 1590-1874; 1590-3478
• DOI: 10.1007/s10072-012-1246-z

Minocycline has shown anti-inflammatory, anti-apoptotic, and antioxidative activities in many models of cerebral ischemia and human acute ischemic stroke. However, the cellular and molecular bases for its neuroprotective effects have not been fully elucidated. In this study, we investigated whether pre-treatment with minocycline could attenuate oxygen-glucose deprivation-induced PC12 cytotoxicity. The activity of matrix metalloproteinase-9 was detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis zymography. And the expressions of integrin beta 1, Akt and phosphorylated Akt were analyzed by Western blot. Our results showed that minocycline could ameliorate oxygen-glucose deprivation-induced PC12 cell cytotoxicity at concentrations of 20 nM-20 mu M, down-regulate the production and activity of matrix metalloproteinase-9, inhibit the degradation of integrin beta 1, and up-regulate Akt phosphorylation at optimal concentration of 200 nM. The results may provide a new area for minocycline's therapeutic intervention for improving the outcomes of cerebral ischemia.