Department of General Pathology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Department of Biochemistry, Institute of Chemistry, University of São Paulo, São Paulo, São Paulo, Brazil.
Exp Physiol. 2023 Jan;108(1):146-157. doi: 10.1113/EP090559. Epub 2022 Dec 2.
What is the central question of this study? Peritoneal injury can result in a persistent fibroproliferative process in the abdominal cavity, causing pain and loss of function of internal organs. This study aimed to demonstrate the use of sodium butyrate (NaBu) as a potential agent to attenuate peritoneal fibrosis induced by a synthetic matrix. What is the main finding and its importance? Our findings provide the first evidence that NaBu attenuates the inflammatory, angiogenesis and fibrogenesis axes involved in the formation of peritoneal fibrovascular tissue, indicating the potential of this compound to ameliorate peritoneal fibrosis.
The aim of this study was to identify the bio-efficacy of sodium butyrate (NaBu) on preventing the development of peritoneal fibrovascular tissue induced by implantation of a synthetic matrix in the abdominal cavity. Polyether-polyurethane sponge discs were implanted in the peritoneal cavity of mice, which were treated daily with oral administration of NaBu (100 mg/kg). Control animals received water (100 μl). After 7 days, the implants were removed for assessment of inflammatory, angiogenic and fibrogenic markers. Compared with control values, NaBu treatment decreased mast cell recruitment/activation, inflammatory enzyme activities, levels of pro-inflammatory cytokines, and the proteins p65 and p50 of the nuclear factor-κB pathway. Angiogenesis, as determined by haemoglobin content, vascular endothelial growth factor levels and the number of blood vessels in the implant, was reduced by the treatment. In NaBu-treated animals, the predominant collagen present in the abdominal fibrovascular tissue was thin collagen, whereas in control implants it was thick collagen. Transforming growth factor-β1 levels were also lower in implants of treated animals. Sodium butyrate downregulated the inflammatory, angiogenesis and fibrogenesis axes of the fibroproliferative tissue induced by the intraperitoneal synthetic matrix. This compound has potential to control/regulate chronic inflammation and adverse healing processes in the abdominal cavity.
本研究的核心问题是什么？腹膜损伤可导致腹腔内持续的纤维增生过程，引起疼痛和内脏器官功能丧失。本研究旨在证明丁酸钠（NaBu）作为一种潜在的药物在减轻合成基质诱导的腹膜纤维化中的作用。主要发现及其重要性是什么？我们的研究结果首次提供了证据，表明 NaBu 可减轻涉及腹膜纤维血管组织形成的炎症、血管生成和纤维生成轴，表明该化合物具有改善腹膜纤维化的潜力。
本研究旨在确定丁酸钠（NaBu）对预防腹腔内植入合成基质引起的腹膜纤维血管组织形成的生物疗效。将聚醚-聚氨基甲酸酯海绵片植入小鼠的腹腔内，每天给予口服 NaBu（100mg/kg）治疗。对照组给予水（100μl）。7 天后，取出植入物评估炎症、血管生成和纤维生成标志物。与对照组相比，NaBu 治疗减少了肥大细胞募集/激活、炎症酶活性、促炎细胞因子水平以及核因子-κB 途径的 p65 和 p50 蛋白。处理还降低了植入物中血红蛋白含量、血管内皮生长因子水平和血管数量所代表的血管生成。与对照组相比，NaBu 处理动物的腹部纤维血管组织中存在的主要胶原蛋白是薄胶原蛋白，而在对照组植入物中则是厚胶原蛋白。转化生长因子-β1 水平在处理动物的植入物中也较低。丁酸钠下调了腹膜内合成基质诱导的纤维增生组织的炎症、血管生成和纤维生成轴。这种化合物具有控制/调节腹腔内慢性炎症和不良愈合过程的潜力。
