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Protective effects of perindopril on d-galactose and aluminum trichloride induced neurotoxicity via the apoptosis of mitochondria-mediated intrinsic pathway in the hippocampus of mice.
Brain Res Bull. 2014 Oct; 109:46-53.BR

Abstract

Perindopril, an angiotensin converting enzyme inhibitor, has been reported to improve learning and memory in a mouse or rat model of Alzheimer's disease (AD) induced by injection of beta-amyloid protein. However, the exact mechanism of perindopril on the cognitive deficits is not fully understood. Our previous data have indicated that perindopril improves learning and memory in a mouse model of AD induced by D-galactose (D-gal) and aluminum trichloride (AlCl₃) via inhibition of acetylcholinesterase activity and oxidative stress. Whether perindopril also inhibit apoptosis to prevent cognitive decline remains unknown in mice. Therefore, the present study explored the protective effects of perindopril in the hippocampus of mice further. Perindopril (0.5 mg/kg/day) was administered intragastrically for 60 days after the mice were given a D-gal (150 mg/kg/day) and AlCl₃ (10 mg/kg/day) intraperitoneally for 90 days. Then the expression of Bcl-2, Bax, Fas, FasL, caspase-3, caspase-8 and caspase-9 were analyzed by RT-PCR and western blotting in the hippocampus. Perindopril significantly decreased caspase-3 and caspase-9 activities, and elevated Bcl-2/Bax ratio in the hippocampus. However, the expression of Fas, FasL and caspase-8 did not change in the hippocampus whether treatment with d-gal and AlCl₃ or perindopril. Taken together, the above findings indicated that perindopril inhibited apoptosis in the hippocampus may be another mechanism by which perindopril improves learning and memory functions in d-gal and AlCl₃ treated mice.

Authors+Show Affiliations

Department of Human Anatomy, Histology and Embryology, Institute of Neurobiology, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, China.Department of Human Anatomy, Xi'an Medical University, Xi'an, Shaanxi 710021, China.Department of Human Anatomy, Shaanxi University of Chinese Medicine, Xi'an, Shaanxi 712046, China.Center of Morphology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, China.Department of Human Anatomy, Histology and Embryology, Institute of Neurobiology, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, China.Department of Human Anatomy, Histology and Embryology, Institute of Neurobiology, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, China.Department of Human Anatomy, Histology and Embryology, Institute of Neurobiology, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, China. Electronic address: qianyh38@mail.xjtu.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

25290208

Citation

Yang, Weina, et al. "Protective Effects of Perindopril On D-galactose and Aluminum Trichloride Induced Neurotoxicity Via the Apoptosis of Mitochondria-mediated Intrinsic Pathway in the Hippocampus of Mice." Brain Research Bulletin, vol. 109, 2014, pp. 46-53.
Yang W, Shi L, Chen L, et al. Protective effects of perindopril on d-galactose and aluminum trichloride induced neurotoxicity via the apoptosis of mitochondria-mediated intrinsic pathway in the hippocampus of mice. Brain Res Bull. 2014;109:46-53.
Yang, W., Shi, L., Chen, L., Zhang, B., Ma, K., Liu, Y., & Qian, Y. (2014). Protective effects of perindopril on d-galactose and aluminum trichloride induced neurotoxicity via the apoptosis of mitochondria-mediated intrinsic pathway in the hippocampus of mice. Brain Research Bulletin, 109, 46-53. https://doi.org/10.1016/j.brainresbull.2014.09.010
Yang W, et al. Protective Effects of Perindopril On D-galactose and Aluminum Trichloride Induced Neurotoxicity Via the Apoptosis of Mitochondria-mediated Intrinsic Pathway in the Hippocampus of Mice. Brain Res Bull. 2014;109:46-53. PubMed PMID: 25290208.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective effects of perindopril on d-galactose and aluminum trichloride induced neurotoxicity via the apoptosis of mitochondria-mediated intrinsic pathway in the hippocampus of mice. AU - Yang,Weina, AU - Shi,Lili, AU - Chen,Lianji, AU - Zhang,Bingyi, AU - Ma,Kaige, AU - Liu,Yong, AU - Qian,Yihua, Y1 - 2014/10/05/ PY - 2014/08/28/received PY - 2014/09/22/revised PY - 2014/09/23/accepted PY - 2014/10/8/entrez PY - 2014/10/8/pubmed PY - 2015/7/15/medline KW - Aluminum trichloride KW - Apoptosis KW - Hippocampus KW - Mouse KW - Perindopril KW - d-Galactose SP - 46 EP - 53 JF - Brain research bulletin JO - Brain Res Bull VL - 109 N2 - Perindopril, an angiotensin converting enzyme inhibitor, has been reported to improve learning and memory in a mouse or rat model of Alzheimer's disease (AD) induced by injection of beta-amyloid protein. However, the exact mechanism of perindopril on the cognitive deficits is not fully understood. Our previous data have indicated that perindopril improves learning and memory in a mouse model of AD induced by D-galactose (D-gal) and aluminum trichloride (AlCl₃) via inhibition of acetylcholinesterase activity and oxidative stress. Whether perindopril also inhibit apoptosis to prevent cognitive decline remains unknown in mice. Therefore, the present study explored the protective effects of perindopril in the hippocampus of mice further. Perindopril (0.5 mg/kg/day) was administered intragastrically for 60 days after the mice were given a D-gal (150 mg/kg/day) and AlCl₃ (10 mg/kg/day) intraperitoneally for 90 days. Then the expression of Bcl-2, Bax, Fas, FasL, caspase-3, caspase-8 and caspase-9 were analyzed by RT-PCR and western blotting in the hippocampus. Perindopril significantly decreased caspase-3 and caspase-9 activities, and elevated Bcl-2/Bax ratio in the hippocampus. However, the expression of Fas, FasL and caspase-8 did not change in the hippocampus whether treatment with d-gal and AlCl₃ or perindopril. Taken together, the above findings indicated that perindopril inhibited apoptosis in the hippocampus may be another mechanism by which perindopril improves learning and memory functions in d-gal and AlCl₃ treated mice. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/25290208/Protective_effects_of_perindopril_on_d_galactose_and_aluminum_trichloride_induced_neurotoxicity_via_the_apoptosis_of_mitochondria_mediated_intrinsic_pathway_in_the_hippocampus_of_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(14)00146-4 DB - PRIME DP - Unbound Medicine ER -