Abstract
This study was designed to investigate whether telomerase was involved in the neuroprotective effect of curcumin and Cur1. Alzheimer's disease is a consequence of an imbalance between the generation and clearance of amyloid-beta peptide in the brain. In this study, we used Aβ1-42 (10 µg/ml) to establish a damaged cell model, and curcumin and Cur1 were used in treatment groups. We measured cell survival and cell growth, intracellular oxidative stress and hTERT expression. After RNA interference, the effects of curcumin and Cur1 on cells were verified. Exposure to Aβ1–42 resulted in significant oxidative stress and cell toxicity, and the expression of hTERT was significantly decreased. Curcumin and Cur1 both protected SK-N-SH cells from Aβ1–42 and up-regulated the expression of hTERT. Furthermore, Cur1 demonstrated stronger protective effects than curcumin. However, when telomerase was inhibited by TERT siRNA, the neuroprotection by curcumin and Cur1 were ceased. Our study indicated that the neuroprotective effects of curcumin and Cur1 depend on telomerase, and thus telomerase may be a target for therapeutic effects of curcumin and Cur1.
Highlights
The exact etiology of Alzheimer’s disease (AD) has not been elucidated, the most widely accepted theory is the ‘‘amyloid cascade theory’’, which proposes that AD is a consequence of an imbalance between the generation and clearance of amyloid-beta (Ab) peptide in the brain [1]
Viability of SK-N-SH cells was reduced to approximately 62% of baseline after a 24 h exposure to Ab1–42 (P,0.001) and curcumin and Cur1 protected against reducing in cell viability (Fig. 2A)
We propose that curcumin and Cur1 have no effect on Human telomerase reverse transcriptase (hTERT) up-regulation in normal cells
Summary
The exact etiology of Alzheimer’s disease (AD) has not been elucidated, the most widely accepted theory is the ‘‘amyloid cascade theory’’, which proposes that AD is a consequence of an imbalance between the generation and clearance of amyloid-beta (Ab) peptide in the brain [1]. The Ab-induced oxidative stress hypothesis [3,4] states that Ab and the damage it initiates are the underlying mechanism leading to injurious increase of oxidative stress in AD brain. Animal studies have confirmed neuroprotective effects of the drug in neurodegenerative conditions such as AD [5,6,7]. Curcumin could reduce oxidative damage and alleviate amyloid pathology in AD [7,8,9]. In vivo studies showed that curcumin could promote disaggregation of existing amyloid deposits, prevent aggregation of new amyloid deposits, and reduce amyloid deposits [10]. In our previous study [11], among curcumin and its six derivatives, curcumin and Cur (the 3-methoxy at both ends of benzene ring was removed, but 4hydroxyl retained) (Fig. 1) showed neuroprotective effects
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