Houttuyniae Herba protects rat primary cortical cells from Aβ(25-35)-induced neurotoxicity via regulation of calcium influx and mitochondria-mediated apoptosis.

Amyloid beta (Aβ) fibrils are believed to play a major role in the pathogenesis of Alzheimer's disease. Although the mechanisms underlying Aβ toxicity remain largely unknown, Aβ fibrils disrupt calcium homeostasis and generate free radicals, resulting in oxidative stress, mitochondrial dysfunction, and apoptotic cell death. Houttuyniae Herba, the aerial part of Houttuynia cordata Thunb. (Saururaceae), is a commonly used herb in traditional Asian medicine. It has been reported to have various bioactivities, including antioxidant effects. In the present study, we investigated the protective effect of standardised Houttuyniae Herba water extract (HCW) against Aβ(25-35)-induced neurotoxicity and its possible mechanisms in rat primary cortical cells. Pretreatment with HCW attenuated the cell damage caused by 8 μM Aβ(25-35) exposure, as evidenced by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, a lactate dehydrogenase assay, and microtubule-associated protein 2 immunostaining. Moreover, HCW inhibited the Aβ(25-35)-induced elevation of the intracellular calcium level, reactive oxygen species overproduction, mitochondrial membrane potential disruption, and caspase 3 activation. These results indicate that HCW protects rat primary cortical neurons against Aβ(25-35)-induced toxicity via the regulation of calcium and the inhibition of mitochondria-mediated apoptosis.