Coniferyl aldehyde alleviates LPS-induced WI-38 cell apoptosis and inflammation injury via JAK2–STAT1 pathway in acute pneumonia

Abstract

Pneumonia is a kind of inflammatory disease characterized by pathogen infection of lower respiratory track. Lipopolysaccharide (LPS) is the main bioactive component of Gram-negative bacteria responsible for inflammatory response. Recently, coniferyl aldehyde (CA) has been reported to play a crucial role because of its anti-inflammatory activity. However, the effect and mechanisms of CA in ameliorating symptoms of acute pneumonia remain unknown. Evaluating and identifying the value and exploring the mechanisms of CA on LPS-mediated WI-38 apoptosis and inflammation were the aims of this study. Here, CCK-8 cell viability assay was applied on WI-38 after treatment with or without LPS at different doses of CA to verify that CA can increase LPS-induced cell viability. Then, quantitative polymerase chain reaction (qPCR) and enzyme-linked-immunosorbent serologic assays (ELISA) suggested that LPS treatment dramatically decreased the expression level of IL-10 (anti-inflammatory factor)while strikingly increasing the expression levels of IL-1β, IL-6, and TNF-α (tumor necrosis factor- α; proinflammatory factor) whereas CA treatment attenuates LPS-induced inflammation of WI-38. Further, flow cytometry and Western blot assay verified that LPS treatment dramatically promoted apoptosis of WI-38 cells, while administration of CA notably inhibited apoptosis of WI-38 cells. Moreover, the Western blot assay hinted that CA could inactivate LPS-induced JAK2–STAT1 signaling pathway. These findings indicated that CA could alleviate LPS-mediated WI-38 apoptosis and inflammation injury through JAK2–STAT1 pathway in acute pneumonia.

Sinomenine attenuates lipopolysaccharide‐induced inflammation and apoptosis of WI‐38 cells by reducing glutathione S‐transferase M1 expression

“…We established the inflammatory model using WI-38 cells challenged by LPS, reflected by increase of proinflammatory cytokines and decrease of anti-inflammatory cytokine, which was consistent to previous reports (He et al, 2021;Yang et al, 2021). A previous report suggested that sinomenine could reduce the inflammation in macrophages (Zeng & Tong, 2020).…”

“…Similarly, our study found that sinomenine blunted the inflammation in WI‐38 cells challenged by LPS, indicating its anti‐inflammatory role in WI‐38 cells. Lung cell apoptosis is also an important property in LPS‐induced pediatric pneumonia model (He et al, 2021; Wang, Zhang, & Chen, 2021; Wang, Zhang, Zhao, & Dai, 2021; Yang et al, 2021). Consistent to these reports, this research also found the increased apoptosis in LPS‐challenged WI‐38 cells.…”

Ubiquitin‐specific peptidase 24 accelerates aerobic glycolysis and tumor progression in gastric carcinoma through stabilizing PLK1 to activate NOTCH1

“…The cells were planted in 96‐well plates and then treated according to the experimental requirements 26 . To study cell viability, 10 μL of Cell Counting Kit 8 (CCK8) solution (Goodbio Technology, Wuhan, China) was added to the treated cells and then incubated in an incubator for 1 h. After being put into a microplate meter, the absorbed light was detected at 450 nm, and the cell viability was calculated.…”

“…The cells were planted in 96-well plates and then treated according to the experimental requirements. 26 To study cell viability, 10 μL of Cell…”

Targeting CENPN to inhibit breast cancer progression: insights into cell growth and aerobic glycolysis modulation

“…Cells were seeded at a density of 5 × 10 3 cells per well into 96-well plates. As previously described [23], 10 µL of CCK-8 reagent (cat. no.…”