Spirulina platensis prevents memory impairment in a rat model of D-galactose-induced aging by targeting oxidative stress, neuroinflammation and gut-brain axis

Studies have elucidated that Spirulina platensis has neuroprotective effects by reducing free radicals and oxidative stress. Therefore, this study evaluated the preventive effects of Spirulina platensis against memory dysfunction, and underlying mechanisms in a rat model of D-galactose-induced aging. Forty male Wistar rats were randomly allocated into three groups (n = 10): control (fed a routine diet+ normal saline, subcutaneously); control+ Spirulina platensis group (fed a routine diet containing 5% Spirulina platensis powder + normal saline, subcutaneously); D-galactose group (fed a routine diet + D-galactose); and D-galactose+ Spirulina platensis group (fed a routine diet containing 5% Spirulina platensis powder + D-galactose).

After the end of the sixth week, memory function was evaluated by the passive avoidance test. Finally, rats were euthanized by decapitation. Then, hippocampal oxidative stress and neuroinflammation, and intestinal protein expression of occludin and toll like receptor (TLR) 4 were determined by an ELISA assay, and western blots, respectively.

Spirulina prevented memory dysfunction by increasing step-through latency time of the passive avoidance test in rats that received D-Galactose. Furthermore, spirulina prevented an increase in hippocampal oxidative stress by reducing reactive oxygen species and malondialdehyde and increasing superoxide dismutase. It also prevented neuroinflammation by reducing hippocampal TNF-α and IL-1β concentrations, and prevented a decrease in intestinal occludin, and an increase in intestinal TLR-4 in D-Galactose-injected rats.

Spirulina prevented memory dysfunction in a rat model of D-galactose-induced aging, which could be explained, at least in part, by the inhibition of oxidative stress and neuroinflammation, and the regulation of gut-brain axis. The authors acknowledge the grant support of the Tehran University of Medical Sciences. We utilized DeepSeek for language polishing and grammatical refinement of this manuscript.

This study was supported by Tehran University of Medical Sciences fund (Grant no 1401-4-233-64165). Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran Fatemeh Rahmati-Dehkordi, Javad Fahanik Babaei, Fatemeh Nabavizadeh & Omid Reza Tamtaji Student Research Committee, Kashan University of Medical Sciences, Kashan, Islamic Republic of Iran Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Islamic Republic of Iran Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran Correspondence to Fatemeh Nabavizadeh or Omid Reza Tamtaji. The authors declare no competing interests.

This study also was approved by the Research Ethics Committee of Tehran University of Medical Sciences (IR.TUMS.AEC.1401.172), and was performed in accordance with the Helsinki Declaration and the internationally accepted guidelines for the care and use of laboratory animals. The study is reported in accordance with the ARRIVE guidelines. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.