Wang Chuanqing, Yin Lijun, Fu Pan, Lu Guoping, Zhai Xiaowen, Yang Changsheng
Department of Nosocomial Infection Control and the Clinical Microbiology Laboratory, Children's Hospital of Fudan University, Shanghai 200032, China.
Department of Nosocomial Infection Control, Children's Hospital of Fudan University, Shanghai 200032, China.
Open Med (Wars). 2023 Jul 25;18(1):20230767. doi: 10.1515/med-2023-0767. eCollection 2023.
Two independent experiments were performed with three groups each (sepsis control, sepsis, and sepsis with apoE23 treatment) to investigate the anti-inflammatory effect of apolipoprotein 23 (apoE23) in a mouse model of sepsis induced by . Survival rates; plasma level variations in tumor necrosis factor (TNF)-α, interleukin (IL)-6, and lipopolysaccharide (LPS); S. colony-forming units in the spleen tissue; and mRNA and protein expression levels of low-density lipoprotein receptor (LDLR), LDLR-related protein (LRP), syndecan-1, and scavenger receptor B1 were evaluated in the livers of mice from the three groups. Results found that the survival rate of septic mice treated with apoE23 was 100% within 48 h, while it was only 40% in septic mice without apoE23 treatment ( < 0.001). The plasma LPS, TNF-α, and IL-6 levels and the load in mice in the apoE23-treated group were significantly lower than those in septic mice ( < 0.05). Moreover, apoE23 restored the downregulated expression of LDLR and LRP in the liver tissue of septic mice. So apoE23 exhibits an anti-inflammatory effect in the mouse model of -induced sepsis. Further studies are required to understand the mechanisms underlying the anti-inflammatory effects of apoE23.
进行了两项独立实验,每组有三个亚组(脓毒症对照组、脓毒症组和载脂蛋白E23治疗的脓毒症组),以研究载脂蛋白E23(apoE23)在由[未提及具体诱导因素]诱导的脓毒症小鼠模型中的抗炎作用。评估了三组小鼠肝脏中的存活率;肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6和脂多糖(LPS)的血浆水平变化;脾脏组织中的[未提及具体细菌名称]菌落形成单位;以及低密度脂蛋白受体(LDLR)、LDLR相关蛋白(LRP)、多配体蛋白聚糖-1和清道夫受体B1的mRNA和蛋白质表达水平。结果发现,接受apoE23治疗的脓毒症小鼠在48小时内的存活率为100%,而未接受apoE23治疗的脓毒症小鼠的存活率仅为40%(P<0.001)。apoE23治疗组小鼠的血浆LPS、TNF-α和IL-6水平以及[未提及具体细菌名称]负荷均显著低于脓毒症小鼠(P<0.05)。此外,apoE23恢复了脓毒症小鼠肝脏组织中LDLR和LRP下调的表达。因此,apoE23在[未提及具体诱导因素]诱导的脓毒症小鼠模型中表现出抗炎作用。需要进一步研究以了解apoE23抗炎作用的潜在机制。