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Neuroprotective role of Diosgenin, a NGF stimulator, against Aβ (1–42) induced neurotoxicity in animal model of Alzheimer’s disease

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Abstract

Diosgenin is a neurosteroid derived from the plants and has been previously reported for its numerous health beneficial properties, such as anti-arrhythmic, hypolipidemic, and antiproliferative effects. Although several studies conducted earlier suggested cognition enhancement actions of diosgenin against neurodegenerative disorders, but the molecular mechanisms underlying are not clearly understood. In the present study, we investigated the neuroprotective effect of diosgenin in the Wistar rats that received an intracerebroventricular injection of Amyloid-β (1–42) peptides, representing a rodent model of Alzheimer’s disease (AD). Animals were treated with 100 and 200 mg/kg/p.o of diosgenin for 28 days, followed by Amyloid-β (1–42) peptides infusion. Animals were assessed for the spatial learning and memory by using radial arm maze and passive avoidance task. Subsequently, animals were euthanized and brains were collected for biochemical estimations and histopathological studies. Our results revealed that, diosgenin administration dose dependently improved the spatial learning and memory and protected the animals from Amyloid-β (1–42) peptides induced disrupted cognitive functions. Further, biochemical analysis showed that diosgenin successfully attenuated Amyloid-β (1–42) mediated plaque load, oxidative stress, neuroinflammation and elevated acetylcholinesterase activity. In addition, histopathological evaluation also supported neuroprotective effects of diosgenin in hippocampus of rat brain when assessed using hematoxylin–eosin and Cresyl Violet staining. Thus, the aforementioned effects suggested protective action of diosgenin against Aβ (1–42) induced neuronal damage and thereby can serve as a potential therapeutic candidate for AD.

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Data availability

The datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request.

Abbreviations

1,25D3–MARRS:

1,25D3 -membrane-associated, rapid response steroid-binding protein

ACh:

Acetylcholine

AChE:

Acetylcholinesterase

aCSF:

Artificial cerebrospinal fluid

AD:

Alzheimer’s disease

Akt:

Protein kinase B

ANOVA:

Analysis of variance

AP:

Anterior–posterior

Aβ:

Amyloid beta

BFCN:

Basal forebrain cholinergic neurons

CAT:

Catalase

CMC:

Carboxymethyl cellulose

CV:

Cresyl violet

DTNB:

5,5-dithio-bis-(2-nitrobenzoic acid)

DV:

Dorsal-ventral

EDTA:

Ethylenediamine tetraacetic acid

ELISA:

Enzyme-linked Immune Sorbent Assay

ERK:

Extracellular signal-regulated kinase

GSR:

Glutathione reductase

H&E:

Hematoxylin and eosin

H2O2 :

Hydrogen peroxide

i.c.v:

Intracerebroventricular

IAEC:

Institutional Animal Ethics Committee

IL-6:

Interleukin 6

JNK:

c-Jun N-terminal kinase

MAPK:

Phosphorylated-p38 mitogen activated protein kinase

ML:

Medial-lateral

NADH:

Nicotinamide adenine dinucleotide

NADPH:

Nicotinamide adenine dinucleotide phosphate

NF-κB:

Nuclear factor kappa B

NGF:

Nerve growth factor

p75NTR:

p75 pan neurotrophin receptor

PI3K:

Phosphatidylinositol 3-kinase

RAM:

Radial arm maze

ROS:

Reactive oxygen species

SD:

Standard deviation

SOD:

Superoxide dismutase

TLR:

Toll-like receptor

TNF-α:

Tumour necrosis factor

TrkA:

Tyrosine kinase A receptor

References

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Acknowledgements

We express our gratitude to the Department of Pharmacognosy and Phytochemistry, Department of Pharmacology and Department of Pharmaceutical Biotechnology, JSS College of Pharmacy, Ooty for providing various chemicals and facilities used during the course of the study. This project was financially supported by the Lady Tata Memorial Trust, Mumbai, India with senior research fellowship (SRF).

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Authors

Contributions

SS performed the experiments and was a major contributor in writing the manuscript. JA analyzed and interpreted the raw data regarding the Alzheimer’s disease. SP conceptualized, reviewed and edited the manuscript. SPD reviewed and edited the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Sivasankaran Ponnusankar.

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Ethical approval

All experiments were conducted in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals (National Research Council (US)) and was approved by the Institutional Animal Ethics Committee (IAEC) (JSSCP/IAEC/PhD/Pharmacy Practice/01/2018–19).

Competing Interest

All authors declare that they have no conflict of interest.

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Som, S., Antony, J., Dhanabal, S. et al. Neuroprotective role of Diosgenin, a NGF stimulator, against Aβ (1–42) induced neurotoxicity in animal model of Alzheimer’s disease. Metab Brain Dis 37, 359–372 (2022). https://doi.org/10.1007/s11011-021-00880-8

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  • DOI: https://doi.org/10.1007/s11011-021-00880-8

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