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农冠荣,赵世元▲,何富海,农英德.石仙桃多糖对铜绿假单胞菌致大鼠肺部感染的作用机制研究[J].中国医药科学,2024,14(11):21-24        基金项目:崇左市科技计划项目(崇科20210733)
石仙桃多糖对铜绿假单胞菌致大鼠肺部感染的作用机制研究
Study on the mechanism of action of Pholidota chinensis polysaccharides on Pseudomonas aeruginosa induced pulmonary infection in rats
  
DOI:
中文关键词:  石仙桃多糖;铜绿假单胞菌;肺部感染;肝素结合蛋白;白细胞介素-6
英文关键词:Pholidota chinensis polysaccharides; Pseudomonas aeruginosa; Pulmonary infection; Heparin binding protein; Interleukin-6
作者单位
农冠荣,赵世元▲,何富海,农英德 崇左市人民医院药学部,广西崇左 532200 
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中文摘要:
      [摘要] 目的 探讨石仙桃多糖(PCP)抑制铜绿假单胞菌(PA)致肺部感染模型大鼠作用并初步探讨其可能的作用机制。 方法 制作PA大鼠肺部感染模型,雄性SD大鼠48只,用水合氯醛腹腔注射麻醉,行气管切开术,将PA注射到气管内,将大鼠随机分为PCP高、中、低剂量组和模型组,每组12只;另用未经处理的12只大鼠作为空白对照组。PCP低、中、高剂量组大鼠每天灌胃PCP 15、20、30 mg/kg,共7 d,模型组和空白对照组大鼠每天按5 ml/kg体重灌胃生理盐水。末次用药后次日用水合氯醛腹腔注射麻醉大鼠,采集肺组织及肺泡灌洗液,测定肺组织湿/干比,计数各组支气管肺泡灌洗液(BALF)的白细胞总数,BALF离心取上清液检测肝素结合蛋白、白细胞介素-6(IL-6)、降钙素原(PCT)细胞因子表达水平,用免疫印迹法(WB)检测BALF中NF-κB等蛋白磷酸化表达水平。 结果 与空白对照组比较,模型组肺组织湿/干比显著增加(P < 0.05),肺泡灌洗液中白细胞数量明显增加(P < 0.05),肝素结合蛋白、白细胞介素-6、降钙素原等表达明显上升(P < 0.05),并可诱导模型组肺组织NF-κB p65和p-1κBα磷酸化(P < 0.05);用PCP治疗PA致肺部感染SD大鼠模型可明显抑制NF-κB p65和p-1κBα磷酸化(P < 0.05),且低、中、高剂量组作用指标呈梯度改变(P < 0.05)。 结论 PCP对PA引起的大鼠肺部感染模型炎症反应保护作用机制可能通过下调肝素结合蛋白等细胞因子的表达和抑制NF-κB的活化及炎症因子的产生。
英文摘要:
      [Abstract] Objective To explore the inhibitory effect of Pholidota chinensis polysaccharides (PCP) on Pseudomonas aeruginosa (PA) induced pulmonary infection in a rat model and to preliminarily explore its possible mechanism of action. Methods A rat model of PA induced pulmonary infection was established: 48 male SD rats were anesthetized by intraperitoneal injection of chloral hydrate, and tracheostomy was performed, and PA was injected into trachea. Rats were randomly divided into high-dose, medium, and low-dose PCP groups and model groups, with 12 rats in each group, another 12 untreated rats were used as blank control group. Rats in low, medium and high-dose PCP groups were given PCP 15 mg/kg, 20 mg/kg and 30 mg/kg daily by gavage for 7 days, while rats in model group and blank control group were given normal saline by gavage at a weight of 5 ml/kg daily. On the day after the last medication, anesthetized rats were intraperitoneally injected with chloral hydrate. Lung tissue and alveolar lavage fluid were collected, and the wet dry weight ratio of lung tissue was measured. The total number of white blood cells in bronchoalveolar lavage fluid (BALF) of each group was counted. The supernatant of BALF was centrifuged to detect the expression levels of cytokines such as heparin binding protein, interleukin-6 (IL-6), and procalcitonin (PCT). The phosphorylation expression levels of NF-κB and other proteins in BALF were detected using Western blotting (WB). Results Compared with the blank group, the wet dry weight ratio of lung tissue in the model group significantly increased (P < 0.05), the number of white blood cells in alveolar lavage fluid significantly increased (P < 0.05), and the expression of heparin binding protein, interleukin-6, procalcitonin and other proteins significantly increased (P < 0.05), which can induce NF-κB p65 and p-1κB α phosphorylation in the lung tissue of the model group (P < 0.05). PCP treatment of PA induced pulmonary infection in SD rat model can significantly inhibit NF-κB p65 and p-1κB α phosphorylation (P < 0.05), and the indicators of action in the low, medium, and high-dose groups showed a gradient change (P < 0.05). Conclusion The protective mechanism of PCP on the inflammatory response of PA-induced pulmonary infection model in rats may be through down-regulating the expression of cytokines such as heparin-binding protein and inhibiting the activation of NF-κB and the production of inflammatory factors.
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