Matrine alleviates coronary microvascular dysfunction in ischemia with non-obstructive coronary artery disease mice induced by advanced glycation end products inhibition of the reactive oxygen species-mediated endoplasmic reticulum stress in cardiac microvascular endothelial cells.

Objective: To investigate the protective effect of matrine on coronary microvascular dysfunction (CMD) induced by advanced glycation end products (AGEs) in a mouse model of ischemia with non-obstructive coronary artery disease (INOCA), with a focus on the underlying mechanisms, particularly the endoplasmic reticulum (ER) stress protein kinase R-like ER kinase (PERK)/ nuclear factor of activated T-cells (NFAT) signaling pathway.

Methods: An INOCA model was established in mice, and CMD was induced by peritoneal injections of AGEs. Matrine was administered daily intraperitoneal injections.