Baicalin relievesMycoplasma pneumoniaeinfection‑induced lung injury through regulating microRNA‑221 to inhibit the TLR4/NF‑κB signaling pathway

Abstract

Mycoplasma pneumoniae (MP) is a common pathogen that can cause respiratory infections. MP pneumonia (MPP) leads to numerous complications, including lung injury and even death. The present study aimed to investigate the protective effects of Baicalin treatment on MP infection-induced lung injury and the molecular mechanism underlying these effects. Briefly, after mice were infected intranasally by MP and treated with Baicalin (80 mg/kg), serum levels of MP-immunoglobulin M (IgM) were detected by ELISA. The expression levels of C-reactive protein (CRP) in lung tissue were detected by immunohistochemistry and the bronchoalveolar lavage fluid (BALF) was examined by ELISA. Inflammatory factors and inflammatory cells in the BALF were assessed. The expression levels of microRNA (miR)-221 in lung tissue were examined by reverse transcription-quantitative PCR and pathological changes in lung tissue were detected by H&E staining. Cell apoptosis was evaluated by TUNEL assay and the protein expression levels of TLR4, MyD88 and NF-κB were detected by western blotting. Baicalin treatment significantly reduced serum levels of MP-IgM and CRP expression in lung tissue during MP infection. In addition, Baicalin decreased the levels of IL-1β, IL-6, IL-18 and TNF-α in the BALF, and the number of inflammatory cells. Baicalin also reduced the inflammatory infiltration in lung tissue induced by MP infection, improved the pathological changes detected in lung tissue, reduced apoptosis, and downregulated the protein expression levels of TLR4, MyD88 and NF-κB. Furthermore, Baicalin treatment downregulated the expression of miR-221 and the protective effects of Baicalin were attenuated by miR-221 overexpression. In conclusion, Baicalin has a therapeutic effect on mice with MP infection-induced lung injury, which may be related to inhibition of miR-221 expression and regulation of the TLR4/NF-κB signaling pathway.

Baicalin Ameliorates Radiation-Induced Lung Injury by Inhibiting the CysLTs/CysLT1 Signaling Pathway

“…Previous studies have found that IL-6, TNF-α, TGF-β, and IL-1β were elevated in lung inflammation [26,27]. Zhang et al found that BA could reduce the levels of IL-1β, IL-6, TNF-α, and inflammatory infiltration of lung tissue in BALF and improve the pathological changes in lung tissue [28]. is is consistent with the findings of this study that BA could improve the pathological tissue damage of RILI and reduce the levels of TGF-β, TNF-α, IL-6, and IL-1β.…”

Clinical efficacy of budesonide combined with acetylcysteine in the treatment of mycoplasma pneumonia infection

“…28 Overexpression of IL-6 can cause damage to multiple organs and systems. 29 TNF-α, which is mainly derived from macrophages, has a wide range of biological and immune functions. TNF-α can directly damage lung endothelial cells and cause lung tissue injury.…”

“…TNF‐α and IL‐6 are two well‐known pro‐inflammatory cytokines that are thought to be central mediators in the cytokine cascades, and also important cytokines for immune and inflammatory response 28 . Overexpression of IL‐6 can cause damage to multiple organs and systems 29 . TNF‐α, which is mainly derived from macrophages, has a wide range of biological and immune functions.…”

Pharmacological effects of baicalin in lung diseases

“…Another study showed that baicalin might limit protein kinase R-like endoplasmic reticulum kinase (PERK)/eukaryotic translation initiation factor 2 (eIF2) pathway activation, which would then downregulate thioredoxin interacting protein (TXNIP) expression and reduce the activation of the NLRP3 inflammasome, resulting in reduced pyroptosis in macrophages with Mtb infection ( Fu et al, 2021 ). Baicalin relieves Mycoplasma pneumoniae infection-induced lung injury by blocking miRNA-221 to regulate the TLR4/NF-κB signaling pathway ( Zhang et al, 2021c ).…”