Pi-Pa-Run-Fei-Tang alleviates lung injury by modulating IL-6/JAK2/STAT3/IL-17 and PI3K/AKT/NF-κB signaling pathway and balancing Th17 and Treg in murine model of OVA-induced asthma

Jie, Xiao-lu; Luo, Zi-Rui; Yu, Jin; Tong, Zheren; Li, Qiaoqiao; Wu, Jiahui; Tao, Yi; Feng, Peishi; Lan, Jian‐Hui; Wang, Ping

doi:10.1016/j.jep.2023.116719

Cited by 3 publications

(1 citation statement)

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“…Although the roles of SGB in pyroptosis are not the concern of this study, they are worthy of further study. At the same time, stimulation by LPS activated the JAK2/STAT3 and NF-κb pathway to amplify the inflammatory response and directly damage lung tissues [ 31 , 32 ], which was inhibited by SGB also. We partly attributed this pivotal role of SGB to Sirt3, due to the potential relationship between STAT3/ NF-κb and mitochondria [ 33 , 34 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

Stellate Ganglion Block Attenuates LPS-Induced Acute Lung Injury by Activating Sirt3 Regulation of Oxidative Stress and Inflammation

Dai,

Ji,

et al. 2024

Biomedicines

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Stellate ganglion blocks (SGBs) has been applied in clinics to alleviate pain-related syndromes for almost a century. In recent years, it has been reported that SGB can attenuate acute lung injury (ALI) in animals. However, the details of these molecular mechanisms remain complex and unclear. In this study, rats were randomly divided into four groups: group C (receiving no treatment), group NS (receiving the intratracheal instillation of normal saline), group L (receiving the intratracheal instillation of LPS) and group LS (receiving SGB after the intratracheal instillation of LPS). The pathological damage of lung tissue, arterial blood gases, the differentiation of alveolar macrophages (AMs) and inflammatory cytokines (IL-1β, IL-6, IL-10) were detected. Furthermore, the oxidative stress indexes (ROS, CYP-D, T-SOD, Mn-SOD and CAT) in serum and the levels of Sirt3 signaling-associated proteins (JAK2/STAT3, NF-κb p65, CIRP and NLRP3) in the lungs were measured. The results revealed that SGB could attenuate lung tissue damage, improve pulmonary oxygenation, promote the differentiation of AMs to the M2 phenotype, decrease the secretion of IL-1β and IL-6, and increase the secretion of IL-10. Meanwhile, SGB was found to inhibit the production of ROS and CYP-D, and enhance the activities of T-SOD, Mn-SOD and CAT. Furthermore, SGB upregulated Sirt3 and downregulated JAK2/STAT3 and NF-κb p65 phosphorylation, CIRP and NLRP3. Our work revealed that SGB could attenuate LPS-induced ALI by activating the Sirt3-mediated regulation of oxidative stress and pulmonary inflammation; this may shed new light upon the protection of SGB and provide a novel prophylactic strategy for LPS-induced ALI.

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