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Esculentoside A 对脂多糖诱导的小鼠急性肺损伤的保护作用。

Protective effect of esculentoside A on lipopolysaccharide-induced acute lung injury in mice.

机构信息

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, Jilin, PR China.

出版信息

J Surg Res. 2013 Nov;185(1):364-72. doi: 10.1016/j.jss.2013.05.018. Epub 2013 May 29.

Abstract

BACKGROUND

Esculentoside A (EsA) is a saponin isolated from the Chinese herb Phytolacca esculenta. In our study, we sought to investigate the protective effects of EsA on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.

MATERIALS AND METHODS

To determine the effects of EsA on the reduction of histopathologic changes in mice with ALI, inflammatory cell count in bronchoalveolar lavage fluid (BALF) and lung wet-to-dry weight ratio were measured in LPS-challenged mice, and lung histopathologic changes observed via paraffin section were assessed. Next, cytokine production induced by LPS in BALF was measured by enzyme-linked immunosorbent assay. To further study the mechanism of EsA protective effects on ALI, IκBa, p38, and extracellular signal receptor-activated kinase pathways were investigated in lung tissue of mice with ALI.

RESULTS

In the present investigation, EsA showed marked effects by reducing inflammatory infiltration, thickening of the alveolar wall, and pulmonary congestion. Levels of tumor necrosis factor α and interleukin 6 elevated by LPS were significantly decreased in BALF in EsA-pretreated ALI model. Furthermore, EsA significantly suppressed phosphorylation of IκBa, p38, and extracellular signal receptor-activated kinase.

CONCLUSIONS

Taken together, our results suggest that EsA suppressed inflammatory responses in LPS-induced ALI through inhibition of the nuclear factor kappa B and mitogen activated protein kinase signaling pathways. EsA may be a promising potential preventive agent for ALI treatment.

摘要

背景

Esculentoside A(EsA)是从中国草药商陆中分离出的一种皂苷。在我们的研究中,我们试图研究 EsA 对脂多糖(LPS)诱导的急性肺损伤(ALI)小鼠的保护作用。

材料和方法

为了确定 EsA 对 LPS 诱导的 ALI 小鼠组织病理学变化减少的影响,测量了 LPS 挑战小鼠支气管肺泡灌洗液(BALF)中炎性细胞计数和肺湿重/干重比,并通过石蜡切片观察肺组织病理学变化。接下来,通过酶联免疫吸附试验测量 LPS 诱导的 BALF 中细胞因子的产生。为了进一步研究 EsA 对 ALI 的保护作用机制,我们研究了 LPS 诱导的 ALI 小鼠肺组织中 IκBa、p38 和细胞外信号受体激活激酶途径。

结果

在本研究中,EsA 通过减少炎症浸润、肺泡壁增厚和肺充血显示出明显的效果。EsA 预处理 ALI 模型中,BALF 中由 LPS 升高的肿瘤坏死因子α和白细胞介素 6 水平显著降低。此外,EsA 显著抑制了 IκBa、p38 和细胞外信号受体激活激酶的磷酸化。

结论

综上所述,我们的研究结果表明,EsA 通过抑制核因子 kappa B 和丝裂原活化蛋白激酶信号通路抑制 LPS 诱导的 ALI 中的炎症反应。EsA 可能是一种有前途的潜在 ALI 治疗预防剂。

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