Emodin reactivated autophagy and alleviated inflammatory lung injury in mice with lethal endotoxemia

• DOI: 10.1538/expanim.19-0004
• Publication Date: 2019-07-10T18:03:58Z
• Authors: Yan Dong; Li Zhang; Yu Jiang; Jie Dai; Ling Tang; Gang Liu
• Keywords: Inflammation; Lipopolysaccharides; Male; 0301 basic medicine; Mice, Inbred BALB C; 0303 health sciences; Emodin; Original; Acute Lung Injury; Anti-Inflammatory Agents; Endotoxemia; 3. Good health; Disease Models, Animal; Mice; 03 medical and health sciences; Autophagy; Animals

An uncontrolled inflammation induced critical health problems with serious morbidity and death, which namely acute lung injury (ALI). Recently researchs have found the anti-inflammatory effects of emodin. Here, we investigated the potential effects of emodin on a mouse model with a lethal dose of the potential mechanisms and lipopolysaccharide (LPS)-induced inflammatory lung injury in mice. The pulmonary histological abnormalities, the Evans blue's leakage, the myeloperoxidase (MPO) activity, the grades of TNF-α, IL-6, nitric oxide (NO), lactic acid (LA) in lung tissues were determined 18 h post exposure of LPS. Based on the expression of LC3-II with BECN1 was determined using Western blotting. Besides, the LPS-exposed mice for survival rate was monitored. The results indicated that intervention with emodin was important for mitigating LPS-induced pulmonary histological change and LPS-induced leakage of Evans blue, which were associated with suppressed elevation of MPO activity and inhibited up-regulation of TNF-α, IL-6, NO with LA in lung tissues. Moreover, intervention with emodin enhanced the survival rate of LPS-exposed mice. Finally, therapy with emodin increased the LC3 and BECN1 in lungs of LPS-exposed mice. Treatment with 3-MA (the autophagy inhibitor) reversed the beneficial effects of emodin. In conclusion, emodin might provide pharmacological benefits in LPS-induced inflammatory lung injury, and the mechanisms might be related to the restoration of autophagy.