The seed extract of Cassia obtusifolia offers neuroprotection to mouse hippocampal cultures.

The precise causative factors in neurodegenerative diseases such as Alzheimer's (AD) and Parkinson's disease remain elusive, but mechanisms implicated comprise excitotoxicity, mitochondrial dysfunction, and in the case of AD, the amyloid beta peptide (Abeta). Current therapeutic strategies for such disorders are very limited; thus, traditional herbal medicines currently receive increased attention. The seeds of Cassia obtisufolia have long been used in traditional eastern medicine and more recently the ethanolic fraction of the seeds (COE) has been shown to attenuate memory impairments in mice. In this study, we set out to determine the effect of COE (range: 0.1 - 10 microg/ml) on calcium dysregulation and cell death models in mouse primary hippocampal cultures implicated in general neurodegenerative processes and in the pathogenesis of AD: excitotoxicity, mitochondrial dysfunction, and Abeta toxicity. It was found that treatment with COE attenuated secondary Ca2+ dysregulation induced by NMDA (700 microM), while a pre-application of COE also reduced NMDA-induced cell death. Furthermore, COE was neuroprotective against the mitochondrial toxin 3-NP (1 mM), while having no significant effect on cell death induced by incubation with naturally-secreted oligomers of Abeta (8.2 pg/ml). Collectively, these results are important for the therapeutic use of COE in the treatment of neurodegenerative disorders.