[Mechanism of Bushen Antai Infusion Granules in promoting angiogenesis in ox-LDL-induced PMVEC injury model by activating autophagy].

This study aims to explore the mechanism of Bushen Antai Infusion Granules by observing the effects of Bushen Antai Infusion Granules on autophagy and angiogenesis in human placental microvascular endothelial cells(PMVECs) injured by oxidized low-density lipoprotein(ox-LDL). PMVECs were induced by 100 μg·mL~(-1) ox-LDL to establish a model of vascular endothelial cell injury at the maternal-fetal interface. The cells were divided into six groups: normal group, model group(100 μg·mL~(-1) ox-LDL), autophagy inhibition group(100 μg·mL~(-1 )ox-LDL + 10 μmol·L~(-1) AMPK inhibitor compound C), and low, medium, and high-dose groups of Bushen Antai Infusion Granules(100 μg·mL~(-1 )ox-LDL + 2.5%, 5%, and 10% of medicated serum of Bushen Antai Infusion Granules). Cell growth and morphological changes were observed under an inverted microscope. Autophagosomes were detected by MDC staining. Cell viability was detected by CCK-8. Cell migration ability was assessed by the scratch test. Lumen formation ability was tested using Matrigel. The expression of microtubule-associated protein 1A/1B-light chain 3Ⅱ(LC3Ⅱ)/microtubule-associated protein 1A/1B-light chain 3Ⅰ(LC3Ⅰ) and P62 was detected by immunofluorescence and Western blot. Levels of vascular endothelial growth factor(VEGF) and vascular endothelial(VE)-cadherin were determined by ELISA. The results showed that compared with the normal group, the model group had significantly reduced cell viability, tube formation ability, cell migration ability, LC3Ⅱ/LC3Ⅰ expression, P62 expression, and levels of VEGF and VE-cadherin. The number of autophagosomes decreased, the number of cells decreased, and the cells lost their protrusions. Compared with the model group, the autophagy inhibition group had significantly lower cell viability, tube formation ability, and migration ability, along with reduced LC3Ⅱ/LC3Ⅰ expression and levels of VEGF and VE-cadherin. In contrast, each dose group of Bushen Antai Infusion Granules showed significantly increased cell viability, tube formation ability, and migration ability, with elevated LC3Ⅱ/LC3Ⅰ expression and VEGF and VE-cadherin levels. P62 expression was significantly decreased, and the number of autophagosomes was significantly increased. As the concentration of Bushen Antai Infusion Granules increased, the cell morphology gradually returned to normal. In conclusion, ischemic conditions at the maternal-fetal interface lead to weakened autophagy, resulting in impaired angiogenesis at the maternal-fetal interface. Bushen Antai Infusion Granules may promote angiogenesis by activating autophagy, thereby improving ischemic conditions at the maternal-fetal interface.