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Alzheimer’s disease (AD) is a common neurodegenerative disorder without any satisfactory therapeutic approaches. AD is mainly characterized by the deposition of β-amyloid protein (Aβ) and extensive neuronal cell death. Curcumin, with anti-oxidative stress (OS) and cell apoptosis properties, plays essential roles in AD. However, whether bisdemethoxycurcumin (BDMC), a derivative of curcumin, can exert a neuroprotective effect in AD remains to be elucidated.

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Objective: To explore the possible relationship between angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), Tie-2 and vascular endothelial growth factor (VEGF) and radiation brain injury (RBI) and detect the expressions of VEGF, Ang-1, Ang-2 and Tie-2 in co-cultured endothelial cells and astrocytes after an irradiation of X-ray., Methods: Murine brain microvascular endothelial cells bEnd.3 and astrocytes were co-cultured in a Transwell culture plate and then exposed to X-ray at various doses (5, 10, 20 and 30 Gy) and cultured for 24 hours. The group without radiation acted as a control. Western blot was used to detect the expressions of VEGF, Ang-1, Ang-2 and Tie-2., Results: As compared with the control group, the expression of VEGF increased in 5, 10, 20 and 30 Gy dose groups [(1.71 ± 0.11), (2.03 ± 0.05), (2.20 ± 0.06), (2.19 ± 0.08) vs (1.26 ± 0.10), P < 0.05]; the expression of Ang-1 decreased in 5, 10, 20 and 30 Gy dose groups [(2.27 ± 0.07), (2.28 ± 0.06), (2.01 ± 0.05), (1.54 ± 0.08) vs (2.46 ± 0.04), P < 0.05]; the expression of Tie-2 decreased in 5, 10, 20 and 30 Gy dose groups [(2.40 ± 0.10), (2.47 ± 0.06), (1.05 ± 0.09), (1.00 ± 0.08)vs(4.80 ± 0.07), P < 0.05]; the expression of Ang-2 increased in 5 Gy and 10 Gy dose groups [(2.10 ± 0.07), (2.43 ± 0.08)vs (1.69 ± 0.05), P < 0.05] while decreased in 20 Gy and 30 Gy dose groups [(1.12 ± 0.10), (1.21 ± 0.04)vs(1.69 ± 0.05), P < 0.05]., Conclusion: X-ray could differentially affect the expressions of VEGF, Ang-1, Ang-2 and Tie-2 in co-cultured endothelial cells and astrocytes. And the differential expressions of VEGF, Ang-1, Ang-2 and Tie-2 may be related with microvascular injury in RBI.