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Xuebijing protects against lipopolysaccharide-induced lung injury in rabbits.

机译:血必净可预防脂多糖诱发的兔肺损伤。

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摘要

Interleukin (IL)-23 has been identified as a member of the IL-12 cytokine family. It plays an important role in inflammation. To demonstrate the changes of IL-23 in acute lung injury (ALI) and investigate the protective effect of Xuebijing in ALI and the underlying molecular mechanism, ALI was induced by intravenous injection of lipopolysaccharide (LPS, 750 microg/kg). Japanese white rabbits challenged with or without LPS were treated with Xuebijing at the same time or saline. Before and after administration of LPS, arterial blood gas and lung weight gain were examined. Pathological changes of lung tissue were measured by light microscopy. IL-23 in serum was detected by enzyme-linked immunosorbent assay (ELISA). All animals demonstrated drops in arterial oxygen tension (Pao(2)) and oxygenation index (Pao(2)/Fio(2)) after LPS application, which were significantly reversed by Xuebijing treatment. Administration of Xuebijing reduced lung water gain. Histopathological study also indicated that Xuebijing treatment markedly attenuated lung histopathological changes, alveolar hemorrhage and inflammatory cells infiltration. Furthermore, IL-23 was higher than control group after LPS treatment, which could be blunted by Xuebijing. These findings confirmed significant protection by Xuebijing against LPS-induced lung vascular leak and inflammation and implicated inhibition of IL-23 expression a potential role for Xuebijing in the management of ALI.
机译:白介素(IL)-23已被鉴定为IL-12细胞因子家族的成员。它在炎症中起重要作用。为了证明IL-23在急性肺损伤(ALI)中的变化并研究血必净对ALI的保护作用及其潜在的分子机制,通过静脉注射脂多糖(LPS,750 microg / kg)诱导ALI。接受或不接受LPS攻击的日本白兔同时用血必净或生理盐水处理。在给予LPS之前和之后,检查了动脉血气和肺增重。通过光学显微镜测量肺组织的病理变化。通过酶联免疫吸附试验(ELISA)检测血清中的IL-23。所有动物在LPS施用后均表现出动脉血氧张力(Pao(2))和氧合指数(Pao(2)/ Fio(2))下降,血必净治疗可明显逆转。血必净的给药减少了肺水的吸收。组织病理学研究还表明,血必净治疗可明显减轻肺组织病理学变化,肺泡出血和炎性细胞浸润。此外,LPS治疗后IL-23高于对照组,这可能是血必净所致。这些发现证实了血必净对LPS诱导的肺血管渗漏和炎症的显着保护,并且暗示IL-23表达的抑制是血必净在ALI管理中的潜在作用。

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