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Article citations


Sun, G.Y., Chuang, D.Y., Zong, Y.J., et al. (2014) Role of Cytosolic Phospholipase A2 in Oxidative and Inflammatory Signaling Pathways in Different Cell Types in the Central Nervous System. Molecular Neurobiology, 50, 6-14.

has been cited by the following article:

  • TITLE: The Novel cPLA2 Inhibitor AK106-001616 Has a Protective Effect on SOD1G93A-Induced Cell Death in NSC34 Murine Motor Neuron-Like Cell

    AUTHORS: Kazuki Ohuchi, Kazuhiro Tsuruma, Masamitsu Shimazawa, Junji Nakamura, Hideaki Hara

    KEYWORDS: AK106-001616, Amyotrophic Lateral Sclerosis, cPLA2, NSC34, SOD1G93A

    JOURNAL NAME: Pharmacology & Pharmacy, Vol.7 No.5, May 23, 2016

    ABSTRACT: The expression of cytosolic phospholipase A2 (cPLA2) expression is up-regulated in animal model of ALS and in patients with familial amyotrophic lateral sclerosis (fALS). Inhibition of cyclooxygenase 2 (COX2), which is a downstream enzyme of cPLA2, ameliorates the impairment of motor function in the ALS model mice. Therefore, the arachidonic acid cascade, including the cPLA2-COX2 pathway, is an important therapeutic target of ALS. The current study was designed to investigate the potential of AK106-001616, an inhibitor of cPLA2, in protection of motor neuron cell death induced by mutant superoxide dismutase (SOD1G93A). AK106-001616 (1 - 10 μM) protected NSC34 cells (mouse motor neuron like cells) against SOD1G93A-induced motor neuron cell death. Furthermore, aspirin, an inhibitor of COX1/2, reduced the SOD1G93A-induced motor neuron cell death at a concentration that inhibited COX2. Celecoxib, a selective COX2 inhibitor, also reduced the SOD1G93A-induced motor neuron cell death. These results suggest that the arachidonic acid cascade is important for SOD1G93A-induced motor neuron cell death and AK106-001616 has a potent neuroprotective effect against it. AK106-001616 may be a useful therapeutic agent against SOD1G93A-induced ALS.