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抗糖尿病新药(D-Ser2)Oxm 拮抗淀粉样β 蛋白细胞毒性的神经保护 效应观察

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抗糖尿病新药(D-Ser2)Oxm 拮抗淀粉样β 蛋白细胞毒性的神经保护 效应观察. / Han, Y.-F.; Hölscher, Christian; Wang, Z.-J. et al.
In: Acta Physiologica Sinica, Vol. 68, No. 3, 25.06.2016, p. 265-275.

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Han YF, Hölscher C, Wang ZJ, Zhang J, Yuan L, Tong JQ et al. 抗糖尿病新药(D-Ser2)Oxm 拮抗淀粉样β 蛋白细胞毒性的神经保护 效应观察. Acta Physiologica Sinica. 2016 Jun 25;68(3):265-275.

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Han, Y.-F. ; Hölscher, Christian ; Wang, Z.-J. et al. / 抗糖尿病新药(D-Ser2)Oxm 拮抗淀粉样β 蛋白细胞毒性的神经保护 效应观察. In: Acta Physiologica Sinica. 2016 ; Vol. 68, No. 3. pp. 265-275.

Bibtex

@article{15b89a3bf33c46e2accef9678c9d987b,
title = "抗糖尿病新药(D-Ser2)Oxm 拮抗淀粉样β 蛋白细胞毒性的神经保护 效应观察",
abstract = "The accumulation and neurotoxicity of amyloid β protein (Aβ) in the brain is one of major pathological hallmarks of Alzheimer's disease (AD). The effective drugs against Aβ have been still deficient up to now. According to a most recent study, (D-Ser2) Oxm, a new antidiabetic drug, not only improves the disorders in plasma glucose and insulin in type 2 diabetes mellitus (T2DM) rats, but also exerts positive effects on hippocampal neurogenesis and synaptogenesis. However, it is still unclear whether (D-Ser2)Oxm can directly protect cultured neurons against Aβ1-42-induced cytotoxicity. In the present study, we investigated the neuroprotective effects of (D-Ser2)Oxm on the cultured primary hippocampal neurons by testing the cell viability, neuronal apoptosis, mitochondrial membrane potential and intracellular calcium concentration. The results showed that treatment with (D-Ser2)Oxm effectively reversed Aβ1-42-induced decline in cell viability (P < 0.001), and this protective effect could be inhibited by the pretreatment with exendin(9-39), a GLP-1 receptor blocker. (D-Ser2)Oxm treatment also decreased Aβ1-42-induced neuronal early apoptosis and down-regulated apoptotic protein caspase3. Meantime, (D-Ser2)Oxm treatment inhibited Aβ1-42-induced [Ca(2+)]i elevation, mitochondrial membrane potential depolarization, and glycogen synthase kinase-3β (GSK3β) activation. These results suggest that (D-Ser2)Oxm can protect hippocampal neurons against Aβ1-42-induced cytotoxicity and this effect may be related to activation of GLP-1 receptors, regulation of intracellular calcium homeostasis and stabilization of mitochondrial membrane potential.",
keywords = "(D-Ser2)Oxm, amyloid β protein, cellular apoptosis, caspase3, intracellular calcium imaging, mitochondrial membrane potential, GSK3β , hippocampal neuron ",
author = "Y.-F. Han and Christian H{\"o}lscher and Z.-J. Wang and J. Zhang and L. Yuan and J.-Q. Tong and D.-D. Wang and M.-N. Wu and J.-S. Qi",
year = "2016",
month = jun,
day = "25",
language = "Chinese",
volume = "68",
pages = "265--275",
journal = "Acta Physiologica Sinica",
issn = "0371-0874",
publisher = "Kexue Chubaneshe/Science Press",
number = "3",

}

RIS

TY - JOUR

T1 - 抗糖尿病新药(D-Ser2)Oxm 拮抗淀粉样β 蛋白细胞毒性的神经保护 效应观察

AU - Han, Y.-F.

AU - Hölscher, Christian

AU - Wang, Z.-J.

AU - Zhang, J.

AU - Yuan, L.

AU - Tong, J.-Q.

AU - Wang, D.-D.

AU - Wu, M.-N.

AU - Qi, J.-S.

PY - 2016/6/25

Y1 - 2016/6/25

N2 - The accumulation and neurotoxicity of amyloid β protein (Aβ) in the brain is one of major pathological hallmarks of Alzheimer's disease (AD). The effective drugs against Aβ have been still deficient up to now. According to a most recent study, (D-Ser2) Oxm, a new antidiabetic drug, not only improves the disorders in plasma glucose and insulin in type 2 diabetes mellitus (T2DM) rats, but also exerts positive effects on hippocampal neurogenesis and synaptogenesis. However, it is still unclear whether (D-Ser2)Oxm can directly protect cultured neurons against Aβ1-42-induced cytotoxicity. In the present study, we investigated the neuroprotective effects of (D-Ser2)Oxm on the cultured primary hippocampal neurons by testing the cell viability, neuronal apoptosis, mitochondrial membrane potential and intracellular calcium concentration. The results showed that treatment with (D-Ser2)Oxm effectively reversed Aβ1-42-induced decline in cell viability (P < 0.001), and this protective effect could be inhibited by the pretreatment with exendin(9-39), a GLP-1 receptor blocker. (D-Ser2)Oxm treatment also decreased Aβ1-42-induced neuronal early apoptosis and down-regulated apoptotic protein caspase3. Meantime, (D-Ser2)Oxm treatment inhibited Aβ1-42-induced [Ca(2+)]i elevation, mitochondrial membrane potential depolarization, and glycogen synthase kinase-3β (GSK3β) activation. These results suggest that (D-Ser2)Oxm can protect hippocampal neurons against Aβ1-42-induced cytotoxicity and this effect may be related to activation of GLP-1 receptors, regulation of intracellular calcium homeostasis and stabilization of mitochondrial membrane potential.

AB - The accumulation and neurotoxicity of amyloid β protein (Aβ) in the brain is one of major pathological hallmarks of Alzheimer's disease (AD). The effective drugs against Aβ have been still deficient up to now. According to a most recent study, (D-Ser2) Oxm, a new antidiabetic drug, not only improves the disorders in plasma glucose and insulin in type 2 diabetes mellitus (T2DM) rats, but also exerts positive effects on hippocampal neurogenesis and synaptogenesis. However, it is still unclear whether (D-Ser2)Oxm can directly protect cultured neurons against Aβ1-42-induced cytotoxicity. In the present study, we investigated the neuroprotective effects of (D-Ser2)Oxm on the cultured primary hippocampal neurons by testing the cell viability, neuronal apoptosis, mitochondrial membrane potential and intracellular calcium concentration. The results showed that treatment with (D-Ser2)Oxm effectively reversed Aβ1-42-induced decline in cell viability (P < 0.001), and this protective effect could be inhibited by the pretreatment with exendin(9-39), a GLP-1 receptor blocker. (D-Ser2)Oxm treatment also decreased Aβ1-42-induced neuronal early apoptosis and down-regulated apoptotic protein caspase3. Meantime, (D-Ser2)Oxm treatment inhibited Aβ1-42-induced [Ca(2+)]i elevation, mitochondrial membrane potential depolarization, and glycogen synthase kinase-3β (GSK3β) activation. These results suggest that (D-Ser2)Oxm can protect hippocampal neurons against Aβ1-42-induced cytotoxicity and this effect may be related to activation of GLP-1 receptors, regulation of intracellular calcium homeostasis and stabilization of mitochondrial membrane potential.

KW - (D-Ser2)Oxm

KW - amyloid β protein

KW - cellular apoptosis

KW - caspase3

KW - intracellular calcium imaging

KW - mitochondrial membrane potential

KW - GSK3β

KW - hippocampal neuron

M3 - Journal article

VL - 68

SP - 265

EP - 275

JO - Acta Physiologica Sinica

JF - Acta Physiologica Sinica

SN - 0371-0874

IS - 3

ER -