Botulinum Toxin Type A Intralesional Monotherapy for Treating Human Hypertrophic Scar in a Dose-dependent Manner: in an Animal Model

2021 ◽  
Author(s):  
Yawei Li ◽  
Xiaofeng Shan ◽  
Qianying Mao ◽  
Ruolan Xiang ◽  
Zhigang Cai
Keyword(s):  
Animal Model ◽  
Botulinum Toxin ◽  
Hypertrophic Scar ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Dependent Manner ◽  
Dose Dependent

scholarly journals Botulinum toxin type A suppresses pro-fibrotic effects via the JNK signaling pathway in hypertrophic scar fibroblasts

2019 ◽  
Vol 311 (10) ◽  
pp. 807-814 ◽  
Author(s):  
Gil Soon Park ◽  
Min Kyun An ◽  
Ji Ha Yoon ◽  
Seok Soon Park ◽  
Sung Hoon Koh ◽  
...  
Keyword(s):  
Botulinum Toxin ◽  
Signaling Pathway ◽  
Hypertrophic Scar ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

scholarly journals Botulinum toxin type A relieve neuropathic pain by suppressing the expression of CXCL13/CXCR5 and GAT-1 in chronic constriction injury rats

2021 ◽  
Author(s):  
Huilian Bu ◽  
Huilian Bu ◽  
Pengfei Jiao ◽  
Pengfei Jiao ◽  
Xiaochong Fan ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Botulinum Toxin ◽  
Sciatic Nerve ◽  
Analgesic Effect ◽  
Chronic Constriction Injury ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Dependent Manner ◽  
Axon Transport

Abstract Botulinum toxin type A (BTX-A) was widely used to treat neuropathic pain in clinic. The underlying analgesic mechanism of BTX-A involves in axonal transport. The chemokine (C-X-C motif) ligand 13 (CXCL13) and GABA transporter 1 (GAT-1) played important roles in chronic pain. We established a chronic constriction injury (CCI) model. The pain behaviors of rats were measured by testing paw withdrawal thresholds (PWTs) and paw withdrawal latencies (PWLs). The level of proteins was measured by western blots. In our results, the CCI rats showed decrease of PWTs and PWLs, which were relieved by BTX-A. BTX-A reversed the over-expression of CXCL13 and GAT-1 in spinal cord, DRG, sciatic nerve and plantar in CCI rats and characterized in dose-dependent manner. The inhibition of BTX-A on proteins we examined didn’t show significant trend among time points. The analgesic effect of BTX-A disappeared after the axon transport of sciatic nerve blocked by the colchicine. But the PWTs of the colchicine treated CCI rats were higher than non- colchicine-treated CCI rats. Colchicine decreased the levels of CXCL13 and GAT-1 in CCI rats. What’s more, the proteins we examined peaked at the sciatic nerve in the non-colchicine group, but the phenomenon disappeared in the colchicine group. In conclusion, the BTX-A and colchicine relieve neuropathic pain and suppress the increase of CXCL13 and GAT-1. Colchicine prevents the analgesic effect of BTX-A by blocking axon transport. The axon transport may play roles in the peripheral mechanisms of neuropathic pain.

scholarly journals Botulinum toxin type A interrupts autophagic flux of submandibular gland

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Shang Xie ◽  
Hui Xu ◽  
Xiao-Feng Shan ◽  
Zhi-Gang Cai
Keyword(s):  
Botulinum Toxin ◽  
Submandibular Gland ◽  
Western Blotting ◽  
Structural Changes ◽  
Fluorescence Probe ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Autophagic Flux ◽  
Dependent Manner

Abstract Botulinum toxin type A (BTXA) is a neurotoxic protein produced by Clostridium botulinum. Our previous studies demonstrated that BTXA inhibits the secretory function of submandibular gland (SMG) and changes its structure. Several studies reported that SMG damage and repair often occur with autophagy in the rat. However, no studies reported whether secretory inhibition and structural changes of SMG after BTXA injection is related with autophagy. The present study was carried out to explore the association between BTXA injection and autophagy in rat SMG. Western blotting and immunofluorescence were used to detect the expression and distribution of light chain 3 (LC3) in rat SMG. MTS was used to detect the toxicity of BTXA on rat SMG-C6 cell line. GFP-LC3 and Lyso-Tracker Red fluorescence probe were used to assess the levels of autophagosomes and lysosome fusion and the effect of BTXA on autophagic flux in SMG-C6. Western blotting and immunofluorescence results showed that BTXA temporarily increased autophagosomes in rat SMG. MTS results showed that BTXA exerted its toxicity on SMG-C6 in a dose-dependent manner. BTXA increased the number of autophagosomes in SMG-C6; however, most autophagosomes did not colocalize with lysosome. Therefore, we presume that BTXA can change autophagic flux of SMG cells, the mechanism of which might relate with BTXA’s disturbing autophagosome-lysosome fusion.

scholarly journals Effects of Botulinum Toxin Type A on Microvessels in Hypertrophic Scar Models on Rabbit Ears

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Na Zhou ◽  
Dongping Li ◽  
Yanzhu Luo ◽  
Junping Li ◽  
Yuhong Wang
Keyword(s):  
Botulinum Toxin ◽  
Hypertrophic Scar ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Treated Group ◽  
Hematopoietic Progenitor Cell ◽  
Control Group ◽  
Vegf Expression ◽  
Rabbit Ears

Background. Although Botulinum Toxin Type A (BTXA) has been applied to scar prevention and treatment, the mechanisms still require further exploration. Objective. To investigate the effects of BTXA on microvessels in the hypertrophic scar models on rabbit ears. Methods. Eight big-eared New Zealand rabbits (males or females) were selected to establish scar models. One ear of each rabbit (4 models in each ear) was selected randomly to be injected with BTXA immediately after modeling and included in the treated group, while the opposite ear was untreated and included in the control group. The growth of scars in each group was observed and recorded, and 4 rabbits were sacrificed on days 30 and 45 after modeling. Then, scar height was measured by hematoxylin-eosin (HE) staining, vascular endothelial growth factor (VEGF) expression was detected by immunohistochemical (IHC) testing, and microvessel density (MVD) was calculated based on CD34 (human hematopoietic progenitor cell antigen). Results. The wounds in each group were well healed and free from infection or necrosis. On days 30 and 45, the scar height, MVD value, and VEGF expression in the treated group were lower than those in the control group (P<0.05). For the treated group, the above indicators on day 45 were lower than on day 30 (P>0.05). Besides, there was a positive correlation between the MVD value and the VEGF expression in the treated group (P<0.05). Conclusion. The injection of BTXA immediately after modeling inhibits VEGF expression and reduces angiogenesis, thereby inhibiting hypertrophic scar formation.

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