Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan, China.
Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan Polytechnic University, Wuhan, China.
Front Cell Infect Microbiol. 2023 Sep 25;13:1243819. doi: 10.3389/fcimb.2023.1243819. eCollection 2023.
type A is the main cause of necrotic enteritis (NE) in chickens. Since the use of antibiotics in feed is withdrawn, it is imperative to find out suitable alternatives to control NE. Baicalin-aluminum complex is synthesized from baicalin, a flavonoid isolated from Georgi. The present study investigated the effects of baicalin-aluminum on the virulence-associated traits and virulence genes expression of CVCC2030, it also evaluated the therapeutic effect on NE. The results showed that baicalin-aluminum inhibited bacterial hemolytic activity, diminished biofilm formation, attenuated cytotoxicity to Caco-2 cells, downregulated the expression of genes encoding for clostridial toxins and extracellular enzymes such as alpha toxin (CPA), perfringolysin O (PFO), collagenase (ColA), and sialidases (NanI, NanJ). Additionally, baicalin-aluminum was found to negatively regulate the expression of genes involved in quorum sensing (QS) communication, including genes of Agr QS system (, ) and genes of VirS/R two-component regulatory system (, ). experiments, baicalin-aluminum lightened the intestinal lesions and histological damage, it inhibited pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) expression in the jejunal and ileal tissues. Besides, baicalin-aluminum alleviated the upregulation of and and raised the relative abundance of in the ileal digesta. This study suggests that baicalin-aluminum may be a potential candidate against infection by inhibiting the virulence-associated traits and virulence genes expression.
A 型产气荚膜梭菌是引起鸡坏死性肠炎（NE）的主要原因。由于饲料中抗生素的使用被禁止，因此必须找到合适的替代品来控制 NE。黄芩素-铝复合物是由黄芩素合成的，黄芩素是从 Georgi 中分离出来的一种黄酮类化合物。本研究探讨了黄芩素-铝对 CVCC2030 毒力相关特性和毒力基因表达的影响，还评估了其对 NE 的治疗效果。结果表明，黄芩素-铝抑制了细菌的溶血活性，减少了生物膜的形成，减弱了对 Caco-2 细胞的细胞毒性，下调了编码梭菌毒素和细胞外酶的基因表达，如α毒素（CPA）、产气荚膜梭菌α毒素（PFO）、胶原酶（ColA）和唾液酸酶（NanI、NanJ）。此外，还发现黄芩素-铝负调控群体感应（QS）通讯相关基因的表达，包括 Agr QS 系统的基因（、）和 VirS/R 双组分调控系统的基因（、）。体内实验表明，黄芩素-铝减轻了肠道病变和组织损伤，抑制了空肠和回肠组织中促炎细胞因子（TNF-α、IL-1β、IL-6）的表达。此外，黄芩素-铝还缓解了 和 的上调，并提高了回肠内容物中 的相对丰度。本研究表明，黄芩素-铝可能通过抑制毒力相关特性和毒力基因表达，成为一种有潜力的抗 感染的候选药物。
