OBJECTIVE:To explore the effect and mechanism of baicalin in the treatment of acute lung injury(ALI)by in vivo and in vitro experiments.METHODS:ALI was induced by instilling 10 mg/m L lipopolysaccharide(LPS)into the a...OBJECTIVE:To explore the effect and mechanism of baicalin in the treatment of acute lung injury(ALI)by in vivo and in vitro experiments.METHODS:ALI was induced by instilling 10 mg/m L lipopolysaccharide(LPS)into the airway of rats.Different doses of baicalin(50 and 100 mg·kg^(-1)·d^(-1 ))were administered by gavage one day before modeling.RESULTS:Baicalin significantly reduced the permeability of the alveolocapillary membrane,alleviated tissue injury and inflammatory infiltration,and inhibited the secretion of inflammatory factors and the infiltration of neutrophils.The decline in these inflammations was related to the inhibition of the toll like receptor-4(TLR4)/myeloid differentiation factor 88(My D88)/nuclear factor-kappa B(NF-κB)/nod-like receptor pyrin containing 3(NLRP3)signaling pathway and the mitogen-activated protein kinase(MAPK)signaling pathway.CONCLUSIONS:Baicalin inhibits the secretion of inflammatory factors by inhibiting the TLR4-My D88-NF-κB/NLRP3 pathway and the MAPK signaling pathway.Thus,it reduces lung bronchial epithelial layer,alveolar damage,and pulmonary edema as detected in the in vivo and in vitro experiments.Therefore,baicalin may be a potential preventive and therapeutic drug for ALI.展开更多
基金Supported by the National Natural Science Foundation of China:Study on the Intervention of Qingjin Huatan Decoction on Hypersecretion of Airway Mucus(81473655)Comparative Study about Intervention of Yupingfeng Powder and Modified Guomin Decoction on Decreased Alveolar Macrophage Phagocytosis and Immune Imbalance Leading to Pulmonary Inflammation Induced by PM2(581673921)。
文摘OBJECTIVE:To explore the effect and mechanism of baicalin in the treatment of acute lung injury(ALI)by in vivo and in vitro experiments.METHODS:ALI was induced by instilling 10 mg/m L lipopolysaccharide(LPS)into the airway of rats.Different doses of baicalin(50 and 100 mg·kg^(-1)·d^(-1 ))were administered by gavage one day before modeling.RESULTS:Baicalin significantly reduced the permeability of the alveolocapillary membrane,alleviated tissue injury and inflammatory infiltration,and inhibited the secretion of inflammatory factors and the infiltration of neutrophils.The decline in these inflammations was related to the inhibition of the toll like receptor-4(TLR4)/myeloid differentiation factor 88(My D88)/nuclear factor-kappa B(NF-κB)/nod-like receptor pyrin containing 3(NLRP3)signaling pathway and the mitogen-activated protein kinase(MAPK)signaling pathway.CONCLUSIONS:Baicalin inhibits the secretion of inflammatory factors by inhibiting the TLR4-My D88-NF-κB/NLRP3 pathway and the MAPK signaling pathway.Thus,it reduces lung bronchial epithelial layer,alveolar damage,and pulmonary edema as detected in the in vivo and in vitro experiments.Therefore,baicalin may be a potential preventive and therapeutic drug for ALI.
