Berberine Ameliorates Inflammation in Acute Lung Injury via NF-κB/Nlrp3 Signaling Pathway

Jiyu Chen; Yanli Huang; Xiaohong Bian; Yan He

doi:10.3389/fnut.2022.851255

Berberine Ameliorates Inflammation in Acute Lung Injury via NF-κB/Nlrp3 Signaling Pathway

Front Nutr. 2022 Feb 25:9:851255. doi: 10.3389/fnut.2022.851255. eCollection 2022.

Authors

Jiyu Chen¹, Yanli Huang², Xiaohong Bian³, Yan He¹

Affiliations

¹ Clinical Trials Center, The Affiliated Hospital of Guizhou Medical University, Guiyang, China.
² Office of Academic Research, The Affiliated Hospital of Guizhou Medical University, Guiyang, China.
³ School of Life Science and Technology, China Pharmaceutical University, Nanjing, China.

Abstract

The inflammatory response is the key pathophysiological character of acute lung injury (ALI). Berberine (BBR), a natural quaternary ammonium alkaloid, plays a functional role in anti-inflammation both in vitro and in vivo. However, the underlying mechanism between BBR and ALI has not been expounded. Here, we found that BBR improved the permeability of pulmonary and repressed the inflammatory factors in the lipopolysaccharides (LPSs)-induced ALI model. We demonstrated that BBR could suppress the expression of phosphorylated nuclear factor-kappa B (NF-κB) and further restrain the downstream gene nucleotide-binding domain and leucine-rich repeat protein-3 (Nlrp3). Moreover, we also revealed that BBR could directly interact with Nlrp3 protein. After knocked down of Nlrp3 by using siRNA, the protective role of BBR was abrogated in vitro. The expression of IL-1β and IL-18 was downregulated by BBR via the two signaling pathways. Notably, in Nlrp3 deficient mice, the protective effect of BBR was abolished. These findings demonstrate that BBR has a depressant effect on inflammatory response caused by LPS via regulating NF-κB/Nlrp3 signaling pathway, providing a potential therapeutic strategy in ALI.

Keywords: ALI; NF-κB; Nlrp3; berberine; inflammation.