NEUROPROTECTIVE EFFECT OF TERMINALIA CHEBULA EXTRACTS AND ELLAGIC ACID IN PC12 CELLS.

BACKGROUND: Alzheimer's disease (AD) is one of the common neurodegenerative disorders among elderly. The purpose of this study was to determine the neuroprotective effect and mechanisms of action underlying the Terminalia chebula extracts and ellagic acid by using beta-amyloid25-35 (Aß25-35)-induced cell toxicity in an undifferentiated pheochromocytoma (PC12) cell line. MATERIALS AND METHODS: The T. chebula extracts were prepared using the methanol, water, and 95% ethanol. Specifically, the ellagic acid was obtained in our laboratory. Assays including cell toxicity and changes in intracellular reactive oxygen species (ROS) and calcium level were evaluated to examine the neuroprotective effects and mechanisms of the T. chebula extracts and ellagic acid. RESULTS: The methanolic and water extracts of T. chebula and ellagic acid exhibited the strongest neuroprotective activity against Aß25-35-induced PC12 cell damages at 0.5-5.0 µg/ml. The ellagic acid also exhibited partial neuroprotective activity against H2O2-induced PC12 cell damages at 0.5-5.0 µg/ml. The methanolic and water extracts of T. chebula and ellagic acid protected PC12 cells from Aß25-35-mediated cell damages and enhanced cell viability thorough two key mechanisms by: (1) inhibiting ROS production and (2) reducing calcium ion influx. CONCLUSION: The T. chebula represents a promising plant-source as medicine in the application for the treatment of AD. Further investigation focusing on the active component of T. chebula extracts e.g., ellagic acid is crucial to verify the neuroprotective efficacy and mechanisms in vivo.

Phytochemical characteristics, free radical scavenging activities, and neuroprotection of five medicinal plant extracts.

The objective of this study was to determine phytochemical characteristics, chemiluminescence antioxidant capacities, and neuroprotective effects on PC12 cells for methanol extracts of Spatholobus suberectus, Uncaria rhynchophylla, Alpinia officinarum, Drynaria fortunei, and Crataegus pinnatifida. The C. pinnatifida extract (CPE) afforded the greatest yield and total phenolic content. The S. suberectus extract (SSE) yielded the greatest total flavonoid content. The U. rhynchophylla extract (URE) produced the greatest total tannin content, and the A. officinarum extract (AOE) produced the greatest total triterpenoid content. The D. fortunei extract, assayed using horseradish peroxidase-luminol-hydrogen peroxide (H(2)O(2)), and AOE using pyrogallol-luminol assay each exhibited better antioxidant activity than the L-ascorbic acid and 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid did. The CPE, SSE, and URE presented neurogrowth effects and neuroprotective activities on H(2)O(2)-induced PC12 cell death at 0.5-5.0 µg/mL. The CPE represents a promising medicinal plant source for the treatment of H(2)O(2)-induced neurodegenerative disease, because of its useful phytochemical characteristics.

Phytochemical Composition, Antioxidant Activity, and Neuroprotective Effect of Terminalia chebula Retzius Extracts.

The objectives of this study were to determine phytochemical compositions, chemiluminescence antioxidant activities, and neuroprotective effects on PC12 cells for water, methanol, and 95% ethanol extracts of the air-dried fruit of Terminalia chebula Retzius. The water extract afforded the greatest yield, and total phenolic and tannin content. The methanol extract yielded the greatest total triterpenoid content. Based on four chemiluminescence antioxidant assays, the three extracts showed various degrees of antioxidant activity. The methanol extract showed good antioxidant activity based on the horseradish peroxidase-luminol-hydrogen peroxide (H(2)O(2)) assay. The water extract appeared to have good antioxidant activities in cupric sulfate-Phen-Vc-H(2)O(2) and luminol-H(2)O(2) assays. Pyrogallol-luminol assay showed the 95% ethanol extract to have good antioxidant activity. The methanol and water extracts presented neuroprotective activities on H(2)O(2)-induced PC12 cell death at 0.5-5.0 µg/mL. Further investigations are necessary to verify these activities in vivo.