Neurodegenerative disorders, e.g., Alzheimer’s disease (AD) and Parkinson’s disease (PD)
are characterized by the progressive loss of neurons and subsequent cognitive decline. They are mainly
found in older populations. Due to increasing life expectancies, the toll inflicted upon society by these
disorders continues to become heavier and more prominent. Despite extensive research, however, the
exact etiology of these disorders is still unknown, though the pathophysiological mechanisms have
been attributed to oxidative, inflammatory and apoptotic injury in the brain. Moreover, there is currently
no promising therapeutic agent against these neurodegenerative changes. Catalpol, an iridoid glucoside contained
richly in the roots of the small flowering plant species Rehmannia glutinosa Libosch, has been shown to have antioxidation,
anti-inflammation, anti-apoptosis and other neuroprotective properties and plays a role in neuroprotection
against hypoxic/ischemic injury, AD and PD in both in vivo and in vitro models. It may therefore represent a potential
therapeutical agent for the treatment of hypoxic/ischemic injury and neurodegenerative diseases. Based on our studies and
those of others in the literature, here we comprehensively review the role of Catalpol in neuroprotection against pathological
conditions, especially in neurodegenerative states and the potential mechanisms involved.
Keywords: Catalpol, neurodegenerative disease, neuroprotection, oxidant stress, inflammation, mitochondria, NF-κB, neurotrophins.
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