The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China.
The Key Laboratory of Hunan Province for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of Cardio-Cerebral Diseases, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China, China.
Biomed Pharmacother. 2017 Dec;96:148-152. doi: 10.1016/j.biopha.2017.09.094. Epub 2017 Sep 30.
Acute lung injury (ALI) and its severe form acute respiratory distress syndrome remain the leading cause of morbidity and mortality. LianQinJieDu (LQJD), which is a traditional Chinese medicine, has been clinically used for antiviral drug. The present study investigated whether Lianqinjiedu(LQJD) ameliorates lipopolysaccharide(LPS)-induced acute lung injury in rats and aimed to determine the anti-inflammatory effects of LQJD. Rat model with ALI induced by intraperitoneal injection of LPS was treated by oral administration of LQJD. The recruitment of body temperature and the histopathology of lung tissue from all groups were evaluated to grade the severity of the inflammation. The inflammatory cytokine levels, including tumor necrosis factor-α (TNF-α)and interleukin-6 (IL-6), were examined by ELISA assay, and the TLR4 and NF-κBp65 expression levels were evaluated by Real time-PCR and western blotting. It was observed that LQJD reduced the LPS-induced body temperature, inflammatory cytokines level, and lung injuries, and blocked the activation of TLR4/NF-κBp65 signaling in lung tissue. This study demonstrates that LQJD has a protective effect on LPS-induced inflammatory rats through the signaling pathway of TLR4 and NF-κBp65.
急性肺损伤（ALI）及其严重形式急性呼吸窘迫综合征仍然是发病率和死亡率的主要原因。连芩解毒（LQJD）是一种中药，已在临床上用于抗病毒药物。本研究旨在探讨连芩解毒（LQJD）是否能改善脂多糖（LPS）诱导的大鼠急性肺损伤，并确定 LQJD 的抗炎作用。采用腹腔注射 LPS 诱导大鼠 ALI 模型，并用 LQJD 口服治疗。评估各组体温募集情况和肺组织病理变化，以分级炎症严重程度。通过 ELISA 测定肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）等炎症细胞因子水平，并通过实时 PCR 和 Western blot 评估 TLR4 和 NF-κBp65 的表达水平。结果表明，LQJD 降低了 LPS 诱导的体温、炎症细胞因子水平和肺损伤，并阻断了 TLR4/NF-κBp65 信号通路在肺组织中的激活。这项研究表明，LQJD 通过 TLR4 和 NF-κBp65 信号通路对 LPS 诱导的炎症大鼠具有保护作用。
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