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Diphenyl pyrimidine exhibits protective effect on Staphylococcus aureus pneumonia in rat model by targeting NLRP3 expression
Microbial Pathogenesis ( IF 3.8 ) Pub Date : 2021-08-31 , DOI: 10.1016/j.micpath.2021.105168
Wei Duan 1 , Feizhang Qin 2 , Dean Wu 3 , Yunhong Dai 4
Affiliation  

Pneumonia is one of the most frequent disorder induced by S. aureus infection and accounts for 13.3% of the all the infections caused by staphylococcus. In the present study effect of diphenyl pyrimidine was investigated against Staphylococcus aureus (S. aureus) induced pneumonia in the rat model. The results demonstrated that diphenyl pyrimidine treatment of the rats effectively prevented S. aureus induced increase in mortality in dose-dependent manner. Diphenyl pyrimidine treatment inhibited histopathological changes in S. aureus infected rat lungs. Treatment of the rats with 1.25, 2.5, 5 and 10 mg/kg doses of diphenyl pyrimidine significantly (P < 0.05) reversed S. aureus infection induced increase in interleukin (IL)-1β, IL-18 and tumor necrosis factor (TNF)-α levels. Treatment with 1.25, 2.5, 5 and 10 mg/kg doses of diphenyl pyrimidine significantly (P < 0.05) reversed S. aureus infection induced increase nucleotide-binding domain and leucine-rich repeat containing (NLR) protein (NLRP3), apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC) and caspase-1 protein expression in rat lungs in dose-dependent manner. The NLRP3, ASC and caspase-1 mRNA level in S. aureus infected rat pulmonary tissues was significantly (P < 0.05) reduced by diphenyl pyrimidine treatment in dose-dependent manner. Thus, diphenyl pyrimidine protects S. aureus-induced pneumonia through suppression of NLRP3 and inflammatory cytokine expression. Therefore, diphenyl pyrimidine can be of therapeutic importance for the treatment of S. aureus induced pneumonia.



中文翻译:

二苯基嘧啶通过靶向NLRP3表达对大鼠模型金黄色葡萄球菌肺炎具有保护作用

肺炎是金黄色葡萄球菌感染最常见的疾病之一,占葡萄球菌感染的13.3%。在本研究中,在大鼠模型中研究了二苯基嘧啶对金黄色葡萄球菌( S. aureus ) 诱导的肺炎的作用。结果表明,大鼠的二苯基嘧啶处理以剂量依赖性方式有效地防止了金黄色葡萄球菌诱导的死亡率增加。二苯基嘧啶治疗抑制了金黄色葡萄球菌感染的大鼠肺的组织病理学变化。用 1.25、2.5、5 和 10 mg/kg 剂量的二苯基嘧啶处理大鼠显着(P < 0.05)逆转了金黄色葡萄球菌感染诱导白细胞介素 (IL)-1β、IL-18 和肿瘤坏死因子 (TNF)-α 水平增加。用 1.25、2.5、5 和 10 mg/kg 剂量的二苯基嘧啶处理显着 (P < 0.05) 逆转了金黄色葡萄球菌感染诱导的核苷酸结合域和富含亮氨酸重复序列 ( NLR ) 蛋白 ( NLRP3 ) 的增加,与细胞凋亡相关含有 C 端 caspase 募集结构域 (ASC) 的斑点样蛋白和caspase-1蛋白在大鼠肺中以剂量依赖性方式表达。金黄色葡萄球菌中NLRP3ASCcaspase- 1 mRNA 水平二苯基嘧啶处理以剂量依赖性方式显着降低受感染的大鼠肺组织(P < 0.05)。因此,二苯基嘧啶通过抑制NLRP3和炎性细胞因子表达来保护金黄色葡萄球菌诱导的肺炎。因此,二苯基嘧啶对于治疗金黄色葡萄球菌引起的肺炎具有重要的治疗意义。

更新日期:2021-08-31
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