- Meeting abstract
- Open Access
Neuroprotective effects of 3,5-di-o-caffeoylquinic acid in vitro and in vivo
© Han and Isoda; licensee BioMed Central Ltd. 2011
- Published: 22 November 2011
- Neuroprotective Effect
- Moris Water Maze
- SAMP8 Mouse
- Caffeoylquinic Acid
- Glioma Cell Death
Caffeoylquinic acid (CQA) derivatives are natural functional compounds isolated from a variety of plants and possess a broad range of pharmacological properties, including antioxidant, hepatoprotectant, antibacterial, antihistaminic, anticancer, and other biological effects . Recently, it has been demonstrated that CQA derivatives possess neuroprotective effects in Aβ-induced PC12 cell toxicity and in tetrahydropapaveroline (THP)-induced C6 glioma cell death . One of the animal models that is used to study AD and aging is the senescence-accelerated mouse (SAM). The SAM model was developed in 1981, which originally consisted of nine major senescence-accelerated-prone mice (SAMP) substrains and three major senescence-accelerated-resistant mice (SAMR) substrains, each of which exhibits the characteristic disorders.
As in vitro experiment, the human neuroblastoma clonal SH-SY5Y cell were maintained at 37°C under 5% CO2 / 95% air. As in vivo experiment, the CQA-treated mice were orally administered with 3,5-di-O-CQA mixed with drinking water (6.7 mg/kg · day) for 1 month using oral administration tube and syringe. Proteomics analysis, real-time PCR, measurement of intracellular ATP content, Moris water maze were carried out to investigate the neuroprotective effect of CQA.
3,5-di-O-CQA had neuroprotective effect on Aβ1–42 treated cells. The mRNA expression of glycolytic enzyme (phosphoglycerate kinase-1; PGK1) and intracellular ATP level were increased in CQA treated SH-SY5Y cells. We also found that CQA administration induced the improvement of spatial learning and memory on SAMP8 mice, and the overexpression of PGK1 mRNA.
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