原儿茶酸对子宫内膜异位症大鼠炎症反应及血管生成的作用机制研究

doi:10.3969/j.issn.1006-6233.2023.01.015

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Abstract Objective: To observe the effect and mechanism of protocatechuic acid (PA) on angiogenesis in rat endometriosis (EMS). Methods: Fifty-four female SD rats in estrus were selected to establish the EMS disease model by endometrial autograft and the rats were randomly divided into blank group, model group, PA (high, medium and low) dose group and gestrinone group. PA and gestrinone groups were administered gavage once a day. The model group was given the same volume of normal saline for 28 days. The rats in the blank group were fed normally. The ectopic tissue volume of rats was measured, and the tumor necrosis factor in the peritoneal fluid of rats in each group was detected by enzyme-linked immunosorbent assay (ELISA) α (TNF-α), Interleukin 6 (IL-6) and interleukin 1 β (IL-1 β). The levels of angiopoietin (ANG)-1 and Ang-2, the contents of vascular endothelial growth factor (VEGF), matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9) in serum and tissues, and the protein expression of total extracellular signal regulated kinase 1/2(t-ERK1/2) and phosphorylated total extracellular signal regulated kinase 1/2(p-ERK1/2) in tissues were detected by Western blot. Results: Compared with the blank group, the lesion volume increased at 14d and 42d, and the inflammatory factor TNF-α, IL-6, IL-1 β and Ang-1 and Ang-2, VEGF, MMP-2 and MMP-9, p-ERK1/2, VEGF, MMP-2 and MMP-9 in endometriosis were all significantly increased in the model group rats (P<0.05). The changes of the above indexes were negatively regulated in a concentration dependent manner in the low-dose group, the middle dose group and the high-dose group of protocatechuic acid (P<0.05). Conclusion: Protocatechuic acid can reduce wound injury and inhibit inflammatory reaction and angiogenesis in rats with endometriosis. The underlying mechanism may be related to inactivation of ERK / VEGF / MMP pathway.

Key words： Endometriosis Protocatechuic acid Extracellular signal regulated kinase vascular endothelial growth factor matrix metalloproteinase pathway

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2023.01.015 OR http://www.hbyxzzs.cn/EN/Y2023/V29/I1/81

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