Oridonin alleviates lipopolysaccharide-induced acute lung injury in mice through inhibiting apoptosis, oxidative stress, and inflammation by modulating VIP/cAMP/PKA/AQPs signaling pathway

Author:

Liu Qinghua1,Shang Wenli1,Zhang Junli1,Chen Ran1,Wei Li1,Wang HaiDong2,Zhang Min1,Yue Maokui1

Affiliation:

1. The Second Affliated Hospital of Shandong First Medical University

2. Shandong First Medical University

Abstract

Abstract Oridonin (ORI) are a traditional Chinese herbal medicine extracted from Isodon rubescens (Hemsl.) H.Ha. There are few studies on the protective effect of ORI ameliorates acute lung injury (ALI) in mice. This result showed that compared with the ALI group, ORI significantly reduced the total protein content, Wet-to-dry (W/D) ratio, the number of neutrophils, lymphocytes, and monocytes. Moreover, ORI was able to reduce cell apoptosis, the levels of Macrophage inflammatory protein-2 (MIP-2), Intercellular adhesion molecule-1 (ICAM-1), Tumor necrosis factor-α (TNF-α), Malondialdehyde (MDA) and Myeloperoxidase (MPO) and increase the level of Superoxide (SOD). In addition, ORI could up-regulate the levels of VIP, cAMP, p-PKA/PKA and AQP1. In conclusion, our findings indicate that ORI can modulate the inflammatory injury of lung tissue caused by LPS through the VIP/cAMP/PKA/AQPs signaling pathway, suggesting that ORI can be a candidate for the therapeutic or preventive intervention in acute lung inflammation.

Publisher

Research Square Platform LLC

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