Abstract
Botulinum toxin type-A (Btx-A), a powerful therapeutic tool in various medical specialties, requires repeated injections to maintain its effect. Therefore, novel methods to prolong the effective duration time of Btx-A are highly needed. Rats were assigned to three major groups: control group (n = 30), Btx-A group (n = 30), and IGF-1 Ab groups. IGF-1 Ab groups were composed by sub-groups A1–A5 (each has 25 rats) for the subsequent IGF-1Ab dose-effect study. Muscle strength was determined by a survey system for rat lower limbs nerve and muscle function. Muscle-specific receptor tyrosine kinase (MuSK), Insulin-like growth factor binding protein-5 (IGFBP5), and growth-associated protein, 43-kDa (GAP43) were determined by real-time polymerase chain reactions (PCRs) and Western blot. We found that Btx-A decreased the muscle strength, with a paralysis maintained for 70 days. IGF-1Ab prolonged the effective duration time of Btx-A. Real-time PCRs and Western blot showed that IGF-1Ab delayed the increase of MuSK and IGFBP5 after Btx-A injection, without affecting GAP43. These results indicate that IGF-1Ab might prolong the effective duration time of Btx-A on muscle strength through delaying the increase of MuSK. It would be interesting to determine whether IGF-1Ab can be used as an auxiliary measure to the Btx-A treatment in the future.
Highlights
Botulinum toxins (BTs), the exotoxin of the obligate anaerobe Clostridium botulinum, are comprised of a family of seven serotypes (A–G) that block the transmission at neuromuscular junctions (NMJs) by inhibiting quantal acetylcholine (Ach) release [1]
Botulinum toxin type-A (Btx-A) Decreases the Muscle Strength, with a Paralysis Maintained till 70 Days
The muscle strength in Btx-A group remained significantly lower than control until day 56 (p < 0.05)
Summary
Botulinum toxins (BTs), the exotoxin of the obligate anaerobe Clostridium botulinum, are comprised of a family of seven serotypes (A–G) that block the transmission at neuromuscular junctions (NMJs) by inhibiting quantal acetylcholine (Ach) release [1]. As the selective blocking effect of Btx-A usually wears off 3–4 months after muscle tissue injection [4], repeated injections are usually needed to maintain its desired effect. It is well-known that repetitive injection can trigger immune responses and develop resistance to the toxin as well [5]. After the injection of BTs, loss of innervation induces sprouting of motor nerve terminals. These sprouts are the sole synaptic structures undergoing exoendocytosis and are responsible for functional recovery at the onset of repair of nerve-induced muscle twitching [6]. IGF-1 is shown to promote nerve sprouting and sprouts are important for the recovery of NMJs, it remains unclear whether IGF-1Ab could prevent the recovery of NMJs and prolong the effect of Btx-A
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