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.
Highlights
Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative diseases characterized as progressive impairment of cognition and affective disorder
These results demonstrated that treatment with Sodium Tanshinone IIA sulfonate (STS) remarkably reversed the cognition deficits, which was induced by SCOP
A classical AD-like model induced by scopolamine was employed to evaluate the protective effect of STS [11]
Summary
Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative diseases characterized as progressive impairment of cognition and affective disorder. Oxidative stress has been reported to lead to cell death via apoptosis [3] and degeneration of cholinergic nervous system, which result in impairments of cognition and memory [4]. Previous studies have clearly indicated that enhanced level of ACh leads to functional improvement of central cholinergic synapses and protection of neuronal degeneration [6]. Several AChE inhibitors, tacrine, donepezil, galantamine, rivastigmine, and memantine, have proven to improve cognitive deficits. These drugs are not ideal for clinical use due to their side effects, such as hepatotoxicity and adverse gastrointestinal effects [8, 9]. It is critical to discover alternative drugs with cholinomimetic and antioxidative activities for the treatment of AD [10]
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