
Objective To explore the protection mechanisms about Alpinetin to acute human pulmonary microvascular endothelial cells ( HPMECs ) injury. Methods Different concentration of LPS (0. 01,0. 1 ,1. ,10 mg/L) was applied to the HPMECs to induce acute HPMECs injury. The HPMECs mod- els (n =3) were intervened by Alpinetin(40,80,160,320 mg/L) . Normal HPMECs were selected as control group. The viability of HPMECs was observed,mRNA and protein expression of intercellular cell adhesion molecule-1 (ICAM-1) ,TNF-α,APQ-1 were detected. Results Compared with control group, the protein expression of ICAM-1 , TNF-a were increased, the protein and mRNA expression of APQ-1 and the vi- ability of HPMECs were decreased in model group (P <0. 05). Compared with model group,ICAM-1 and TNF-α protein expressions were significantly inhibited in Alpinetin (80,160 mg/L) group, the mRNA and protein expression of APQ-1 and the viability of HPMECs were significantly increased (P <0. 05, P < 0. 01). Conclusion Alpenitin could protect the HPMECs injury by down-regulated protein expression of ICAM-1, TNF-α and up-regulated the mRNA and protein expression of APQ-1.
Tumor Necrosis Factor-alpha, Flavanones, Microvessels, Down-Regulation, Endothelial Cells, Humans, Intercellular Adhesion Molecule-1, Lung, Cells, Cultured
Tumor Necrosis Factor-alpha, Flavanones, Microvessels, Down-Regulation, Endothelial Cells, Humans, Intercellular Adhesion Molecule-1, Lung, Cells, Cultured
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