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Biomed Pharmacother. 2018 Aug;104:530-536. doi: 10.1016/j.biopha.2018.05.040. Epub 2018 May 25.

Tanshinone IIA exerts neuroprotective effects on hippocampus-dependent cognitive impairments in diabetic rats by attenuating ER stress-induced apoptosis.

Author information

1
Department of Pathology, Faculty of Basic Medicine, Hangzhou Medical College, Hangzhou, Zhejiang 310053, PR China.
2
Department of Clinical Laboratorial Examination, Hangzhou Hai Qin Sanatorium, Hangzhou, Zhejiang 310002, PR China.
3
Ocean Research Center of Zhoushan, Zhejiang University, Zhoushan, Zhejiang, 316021, PR China.
4
Department of Pharmacology, Faculty of Basic Medicine, Hangzhou Medical College, Hangzhou, Zhejiang 310053, PR China.
5
Department of Anatomy, Faculty of Basic Medicine, Hangzhou Medical College, Hangzhou, Zhejiang 310053, PR China. Electronic address: xulinhao@hmc.edu.cn.

Abstract

This study aimed to investigate the mechanism by which tanshinone IIA (Tan IIA) suppresses neuronal apoptosis in the hippocampus of diabetic rats. Sprague-Dawley (SD) rats were randomly divided into the following four groups: a control group, a diabetes group and diabetes groups treated with different doses (2 or 4 mg/kg/day) of Tan IIA. Streptozotocin (STZ) was injected into the rats to induce diabetes. Two days after STZ treatment, Tan IIA was intraperitoneally administered to rats in the Tan IIA groups, whereas an equal volume of saline was administered to rats in the control and diabetes groups. After 6 weeks, a one-trial object recognition task and the Morris water maze were applied. The diabetes group displayed notably decreased learning and memory abilities compared with the control group (P < 0.05). Tan IIA rescued hippocampus-dependent memory. Superoxide dismutase (SOD) activity was reduced, and reactive oxygen species (ROS) production, malondialdehyde (MDA) content, and 78-kDa glucose-regulated protein (Grp78), growth arrest and DNA damage-inducible gene 153 (CHOP/GAD153) and cleaved caspase-3 levels were increased in the hippocampus of diabetic rats compared with that of control rats, changes that were accompanied by an increase in neuronal apoptosis in diabetic rats compared with control rats (P < 0.01). However, Tan IIA reduced the MDA content and GRP78 and CHOP expression by inducing SOD activity. Tan IIA attenuated neuronal apoptosis and improved learning and memory by suppressing endoplasmic reticulum (ER) stress activation.

KEYWORDS:

Endoplasmic reticulum stress; Hippocampus; Learning and memory; Tanshinone IIA

PMID:
29800917
DOI:
10.1016/j.biopha.2018.05.040
[Indexed for MEDLINE]

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