Pectolinarin alleviates inflammatory injury in a lipopolysaccharide-induced pneumonia model by inhibition of the TLR4/MyD88/NF-κB pathway.
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Pediatric pneumonia is a significant public health problem in children under-five years of age. Managing inflammation is an attractive approach for pneumonia prevention and therapy. In the present study, we investigated the anti-inflammatory effect of pectolinarin (Pec), a bioactive compound isolated from various medicinal plants, such as Cirsium setidens (Dunn) Nakai and Cirsium chanroenicum, in a lipopolysaccharide (LPS)-induced pneumonia model both in vivo and in vitro. The results suggested that Pec exerted a protective effect against LPS-induced lung inflammatory injury in mice. Pec attenuated inflammatory responses in lung tissues, as reflected by decreased levels of inflammatory cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), as well as reduced infiltration of inflammatory cells in bronchoalveolar lavage fluid (BALF). In vitro assays also proved that Pec treatment inhibited LPS-induced inflammatory responses in mouse alveolar macrophages MH-S cells. Besides, Pec decreased the LPS-induced upregulation of toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), phosphorylated nuclear factor-kappa B (NF-κB) p65, and nuclear NF-κB p65 protein expression in lung tissues and MH-S cells, implying that Pec inhibited LPS-induced activation of the TLR4/MyD88/NF-κB pathway. Overexpression of TLR4 attenuated the anti-inflammatory effect of Pec in LPS-exposed macrophages. In conclusion, Pec exerted a protective effect on LPS-induced pneumonia through its anti-inflammatory activity by inhibition of the TLR4/MyD88/NF-κB pathway. These findings suggest that Pec may serve as a functional food for the prevention and treatment of pneumonia.