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Treatment effects of tanshinone IIA against intracerebroventricular streptozotocin induced memory deficits in mice.
Brain Res. 2016 Jan 15; 1631:137-46.BR

Abstract

Our previous studies demonstrated that tanshinone IIA (tan IIA) has significant protective effects against the neurotoxicity induced by β-amyloid protein (Aβ) in cultured cortical neurons and PC12 cells. This study was designed to investigate the protective effects of tan IIA against memory deficits induced by streptozotocin (STZ) in a model of sporadic Alzheimer's disease (AD). STZ was injected twice intracerebroventrically (3mg/kg ICV) on alternate days (day 1 and day 3) in mice. Daily treatment with tan IIA (20, 40, and 80mg/kg, i.g.) starting from the first dose of STZ for 28 days showed a dose dependent improvement in STZ induced memory deficits as assessed by Morris water maze (MWM) test. Nissl staining results confirmed the protective effects of tan IIA on cerebral cortical and hippocampal neurons damage induced by STZ. In addition, tan IIA markedly reduced STZ induced elevation in acetylcholinesterase (AChE) activity and malondialdehyde (MDA) level, and significantly inhibited STZ induced reduction in superoxide dismutases (SOD) and glutathione peroxidase (GSH-Px) activities in the parietal cortex and hippocampus. Moreover, tan IIA attenuated p38 mitogen activated protein kinase (MAPK) phosphorylation in the parietal cortex and hippocampus. These findings demonstrate that tan IIA prevents STZ induced memory deficits may be attributed to ameliorating neuronal damage, restoring cholinergic function, attenuating oxidative stress and blocking p38 MAPK signal pathway activation. Based on our previous studies, the present study provides further support for the potential use of tan IIA in the treatment of AD.

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, 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.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.School of Pharmacy, 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 Neurology, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, 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. Electronic address: wn_yang@mail.xjtu.edu.cn.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
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26656068

Citation

Liu, Chang, et al. "Treatment Effects of Tanshinone IIA Against Intracerebroventricular Streptozotocin Induced Memory Deficits in Mice." Brain Research, vol. 1631, 2016, pp. 137-46.
Liu C, Wu Y, Zha S, et al. Treatment effects of tanshinone IIA against intracerebroventricular streptozotocin induced memory deficits in mice. Brain Res. 2016;1631:137-46.
Liu, C., Wu, Y., Zha, S., Liu, M., Wang, Y., Yang, G., Ma, K., Fei, Y., Zhang, Y., Hu, X., Yang, W., & Qian, Y. (2016). Treatment effects of tanshinone IIA against intracerebroventricular streptozotocin induced memory deficits in mice. Brain Research, 1631, 137-46. https://doi.org/10.1016/j.brainres.2015.11.040
Liu C, et al. Treatment Effects of Tanshinone IIA Against Intracerebroventricular Streptozotocin Induced Memory Deficits in Mice. Brain Res. 2016 Jan 15;1631:137-46. PubMed PMID: 26656068.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Treatment effects of tanshinone IIA against intracerebroventricular streptozotocin induced memory deficits in mice. AU - Liu,Chang, AU - Wu,Youxuan, AU - Zha,Shuai, AU - Liu,Mengping, AU - Wang,Ying, AU - Yang,Guangde, AU - Ma,Kaige, AU - Fei,Yulang, AU - Zhang,Yaojie, AU - Hu,Xiaodan, AU - Yang,Weina, AU - Qian,Yihua, Y1 - 2015/12/02/ PY - 2015/07/09/received PY - 2015/11/24/revised PY - 2015/11/25/accepted PY - 2015/12/15/entrez PY - 2015/12/15/pubmed PY - 2016/12/15/medline KW - Acetylcholinesterase KW - Memory deficits KW - Oxidative stress KW - Streptozotocin KW - Tanshinone IIA SP - 137 EP - 46 JF - Brain research JO - Brain Res VL - 1631 N2 - Our previous studies demonstrated that tanshinone IIA (tan IIA) has significant protective effects against the neurotoxicity induced by β-amyloid protein (Aβ) in cultured cortical neurons and PC12 cells. This study was designed to investigate the protective effects of tan IIA against memory deficits induced by streptozotocin (STZ) in a model of sporadic Alzheimer's disease (AD). STZ was injected twice intracerebroventrically (3mg/kg ICV) on alternate days (day 1 and day 3) in mice. Daily treatment with tan IIA (20, 40, and 80mg/kg, i.g.) starting from the first dose of STZ for 28 days showed a dose dependent improvement in STZ induced memory deficits as assessed by Morris water maze (MWM) test. Nissl staining results confirmed the protective effects of tan IIA on cerebral cortical and hippocampal neurons damage induced by STZ. In addition, tan IIA markedly reduced STZ induced elevation in acetylcholinesterase (AChE) activity and malondialdehyde (MDA) level, and significantly inhibited STZ induced reduction in superoxide dismutases (SOD) and glutathione peroxidase (GSH-Px) activities in the parietal cortex and hippocampus. Moreover, tan IIA attenuated p38 mitogen activated protein kinase (MAPK) phosphorylation in the parietal cortex and hippocampus. These findings demonstrate that tan IIA prevents STZ induced memory deficits may be attributed to ameliorating neuronal damage, restoring cholinergic function, attenuating oxidative stress and blocking p38 MAPK signal pathway activation. Based on our previous studies, the present study provides further support for the potential use of tan IIA in the treatment of AD. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/26656068/Treatment_effects_of_tanshinone_IIA_against_intracerebroventricular_streptozotocin_induced_memory_deficits_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(15)00904-X DB - PRIME DP - Unbound Medicine ER -