Open AccessHistological and Clinical Findings in Rabbits Sensitized with GM1 Ganglioside
Author(s) -
Ni Komang Sri Dewi Untari,
Kurnia Kusumastuti,
Guritno Suryokusumo,
I Ketut Sudiana,
Tedy Juliandhy
Publication year - 2020
Publication title -
open access macedonian journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.288
H-Index - 17
ISSN - 1857-9655
DOI - 10.3889/oamjms.2020.4871
Subject(s) - medicine , acute motor axonal neuropathy , peripheral neuropathy , guillain barre syndrome , paralysis , plasmapheresis , h&e stain , pathological , flaccid paralysis , ganglioside , pathology , surgery , antibody , immunology , staining , endocrinology , diabetes mellitus , biochemistry , chemistry
BACKGROUND: Acute motor axonal neuropathy (AMAN) is a peripheral nerve disorder that attacks motor axons and occurs acutely. AMAN is one type of Guillain–Barre syndrome (GBS) which often attacks men of productive age. Until now, although patients have undergone intravenous immunoglobulin (IVIG) therapy and/or plasmapheresis, long-standing disability remains a problem. In Indonesia, the availability and cost of these therapies are constraints.
AIM: Our study aimed to find a proper animal model suitable for AMAN and can be executed in our institution, Naval Health Institute with a hope to find new therapeutic modalities in healing with AMAN.
METHODS: GM1 ganglioside immunized in New Zealand male white rabbits with complete Freund’s adjuvant, every 3 weeks until 20 weeks. We evaluated the effects GM1 ganglioside on body weight, functional score, and axon degeneration’s scale. Functional score was examined based on Tarlov’s. Hematoxylin-eosin was used to stain this slide.
RESULTS: Rabbits that being immunized with GM1 ganglioside experience a number of neurological signs and symptoms that resemble AMAN, that is, sluggish righting reflex, muscular weakness, flaccid hyper paralysis, and body weight loss. Pathological examination shows extensive degeneration of peripheral nerves, infiltration of macrophages, and perineuritis.
CONCLUSION: This histological and clinical findings support that this neuropathy is induced by an autoimmune response delivered by cells that respond to gangliosides.