1. Academic Validation
  2. Sodium Tanshinone IIA Sulfonate Attenuates Scopolamine-Induced Cognitive Dysfunctions via Improving Cholinergic System

Sodium Tanshinone IIA Sulfonate Attenuates Scopolamine-Induced Cognitive Dysfunctions via Improving Cholinergic System

  • Biomed Res Int. 2016;2016:9852536. doi: 10.1155/2016/9852536.
Qing-Qing Xu 1 Yi-Jun Xu 1 Cong Yang 1 Ying Tang 2 Lin Li 1 Hao-Bin Cai 1 Bo-Nan Hou 1 Hui-Fang Chen 1 Qi Wang 1 Xu-Guang Shi 3 Shi-Jie Zhang 1
Affiliations

Affiliations

  • 1 Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
  • 2 The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
  • 3 School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Abstract

Sodium Tanshinone IIA sulfonate (STS) is a derivative of Tanshinone IIA (Tan IIA). Tan IIA has been reported to possess neuroprotective effects against Alzheimer's disease (AD). However, whether STS possesses effect on AD remains unclear. This study aims to estimate whether STS could protect against scopolamine- (SCOP-) induced learning and memory deficit in Kunming mice. Morris water maze results showed that oral administration of STS (10 mg/kg and 20 mg/kg) and Donepezil shortened escape latency, increased crossing times of the original position of the platform, and increased the time spent in the target quadrant. STS decreased the activity of acetylcholinesterase (AChE) and increased the activity of choline acetyltransferase (ChAT) in the hippocampus and cortex of SCOP-treated mice. Oxidative stress results showed that STS increased the activity of superoxide dismutase (SOD) and decreased the levels of malondialdehyde (MDA) and Reactive Oxygen Species (ROS) in hippocampus and cortex. In addition, western blot was carried out to detect the expression of Apoptosis related proteins (Bcl-2, Bax, and Caspase-3). STS upregulated the protein expression of Bcl-2 and downregulated the proteins expression of Bax and Caspase-3. These results indicated that STS might become a promising therapeutic candidate for attenuating AD-like pathological dysfunction.

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