Abstract
Botulinum-toxin A (BoNT/A) is a widely used not only for cosmetics but also for various experimental purposes including muscle-related research. In this study, we applied BoNT/A to mouse muscle of three different sources to compare and evaluate the biological and pathological response. The three different mouse sources consist of Korl:ICR (Korea FDA source), A:ICR (USA source) and B:ICR (Japan source) which were purchased from each different vendors. To compare the responses of ICR mice with BoNT/A muscle injection, we examined the body weight, hematological and serum biochemistry analysis. Also, we evaluated the muscle change by histopathological analysis and gene expression patterns of muscle-related target by qPCR. The body weight gain was decreased in the BoNT/A-treated group compared with the control group. In clinical pathologic analysis and gene expression patterns, the data showed that the responses in the BoNT/A-treated group were similar compared with the control group. Decreased muscle fiber was observed in BoNT/A-treated group compared with control group, while Korl:ICR showed a little low response with the other mouse sources. In conclusion, our results suggest that three different sources ICR mice (Korl:ICR, A:ICR and B:ICR) have a similar biological and pathological responses in BoNT/A muscle injection.
Highlights
Botulinum toxin is known to be one of the most potent toxins in nature [1, 2]
On day 3, mice in the Botulinum-toxin A (BoNT/A)-treated groups had decreased body weight, the differences were not significant compared to the negative control groups
This data showed that the BoNT/A-treated mice experienced a weight loss of approximately 4% compared to the negative control groups
Summary
Botulinum toxin is known to be one of the most potent toxins in nature [1, 2]. Human casualties due to botulinum toxin are reported every year. Botulinum toxin is a type of protein released by a bacterium known as Clostridium botulinum; it acts by reversibly binding to nerves synapses, inhibiting the release of acetylcholine at nerve junctions [11]. This blocks muscle contractions, resulting in secondary muscle relaxation effects, this property has been exploited in the treatment of muscle tension-related diseases [9]
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