Neuroprotective Effect of Bean Phosphatidylserine on TMT-Induced Memory Deficits in a Rat Model

Int J Mol Sci. 2020 Jul 11;21(14):4901. doi: 10.3390/ijms21144901.

Abstract

Background: Trimethyltin (TMT) is a potent neurotoxin affecting various regions of the central nervous system, including the neocortex, the cerebellum, and the hippocampus. Phosphatidylserine (PS) is a membrane phospholipid, which is vital to brain cells. We analyzed the neuroprotective effects of soybean-derived phosphatidylserine (Bean-PS) on cognitive function, changes in the central cholinergic systems, and neural activity in TMT-induced memory deficits in a rat model.

Methods: The rats were randomly divided into an untreated normal group, a TMT group (injected with TMT + vehicle), and a group injected with TMT + Bean-PS. The rats were treated with 10% hexane (TMT group) or TMT + Bean-PS (50 mg·kg-1, oral administration (p.o.)) daily for 21 days, following a single injection of TMT (8.0 mg/kg, intraperitoneally (i.p.)). The cognitive function of Bean-PS was assessed using the Morris water maze (MWM) test and a passive avoidance task (PAT). The expression of acetylcholine transferase (ChAT) and acetylcholinesterase (AchE) in the hippocampus was assessed via immunohistochemistry. A positron emission tomography (PET) scan was used to measure the glucose uptake in the rat brain.

Results: Treatment with Bean-PS enhanced memory function in the Morris water maze (MWM) test. Consistent with the behavioral results, treatment with Bean-PS diminished the damage to cholinergic cells in the hippocampus, in contrast to those of the TMT group. The TMT+Bean-PS group showed elevated glucose uptake in the frontal lobe of the rat brain.

Conclusion: These results demonstrate that Bean-PS protects against TMT-induced learning and memory impairment. As such, Bean-PS represents a potential treatment for neurodegenerative disorders, such as Alzheimer's disease.

Keywords: bean phosphatidylserine (Bean-PS); choline acetyltransferase (ChAT); neurodegenerative disorder; neuroprotection; trimethyltin (TMT).

MeSH terms

  • Acetylcholinesterase / biosynthesis
  • Acetylcholinesterase / genetics
  • Animals
  • Avoidance Learning / drug effects
  • Brain / diagnostic imaging
  • Brain / metabolism
  • Choline O-Acetyltransferase / biosynthesis
  • Choline O-Acetyltransferase / genetics
  • Cognition Disorders / chemically induced
  • Cognition Disorders / prevention & control*
  • Escape Reaction / drug effects
  • Glucose / pharmacokinetics
  • Glycine max / chemistry
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Male
  • Morris Water Maze Test / drug effects
  • Nerve Tissue Proteins / biosynthesis
  • Nerve Tissue Proteins / genetics
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use*
  • Phosphatidylserines / pharmacology
  • Phosphatidylserines / therapeutic use*
  • Positron-Emission Tomography
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Trimethyltin Compounds / toxicity

Substances

  • Nerve Tissue Proteins
  • Neuroprotective Agents
  • Phosphatidylserines
  • Trimethyltin Compounds
  • trimethyltin
  • Choline O-Acetyltransferase
  • Acetylcholinesterase
  • Glucose