[Baicalin alleviates LPS-induced acute lung injury in rats by regulating macrophage polarization]

Objective To investigate the effect of baicalin on acute lung injury (ALI) induced by lipopolysaccharide (LPS), and to explore the roles of M1/M2 polarization of pulmonary macrophages and M1/M2 macrophage-mediated inflammation in the effect. Methods Sixty SD rats were divided into six groups: normal control group, LPS group, (10, 50, 100) mg/kg baicalin combined with LPS group, and dexamethasone (DEX) group. ALI models were established by intratracheal instillation of LPS. After 24 hours, bronchoalveolar lavage fluid (BALF) and bilateral lung tissues were collected. The pathological changes of rat lung tissue were observed by HE staining, and the wet/dry mass ratio (W/D) of lung tissue was measured; the contents of IL-1β, IL-6, TNF-α, and IL-10 in BALF were detected by ELISA; the M1 macrophage marker inducible nitric oxide synthase (iNOS) and the M2 macrophage marker CD206 in CD68 positive macrophages were detected by immunofluorescence cytochemical staining; the mRNA expressions of iNOS, IL-1β, Arg1, and CD206 were detected by real-time PCR, and the protein expressions of iNOS and Arg1 were detected by Western blot analysis. Results Baicalin significantly reduced lung lesions and lung water content in ALI rats, and down-regulated the secretion levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β, while up-regulated the secretion of anti-inflammatory cytokine IL-10 in BALF. Baicalin significantly inhibited the lung macrophage polarization to M1 phenotype, and promoted the polarization to M2 phenotype. Baicalin significantly decreased the mRNA and protein expression levels of IL-1β and iNOS, while increased the mRNA and protein expression levels of CD206 and Arg1 in lung tissues. Conclusion Baicalin can inhibit the lung macrophage polarization to M1 phenotype, promote the polarization to M2 phenotype, and reduce the M1/M2 ratio, thereby alleviating the LPS-induced pulmonary inflammatory response in ALI rats.