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Abstract Title:

Treatment effects of tanshinone IIA against intracerebroventricular streptozotocin induced memory deficits in mice.

Abstract Source:

Brain Res. 2016 Jan 15 ;1631:137-46. Epub 2015 Dec 2. PMID: 26656068

Abstract Author(s):

Chang Liu, Youxuan Wu, Shuai Zha, Mengping Liu, Ying Wang, Guangde Yang, Kaige Ma, Yulang Fei, Yaojie Zhang, Xiaodan Hu, Weina Yang, Yihua Qian

Article Affiliation:

Chang Liu

Abstract:

Our previous studies demonstrated that tanshinone IIA (tan IIA) has significant protective effects against the neurotoxicity induced byβ-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 ofAD.

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