Pericardial adipose tissue-derived leptin promotes myocardial apoptosis in high fat diet-induced obese rats through JAK2/ROS/NKA signaling pathway

Abstract Background Pathophysiologic mechanisms underlying cardiac structural and functional changes in obesity are complex linked to adipocytokines released from pericardial adipose tissue (PAT) cardiomyocyte apoptosis. Although leptin is involved various pathological conditions, its role paracrine action of on myocardial apoptosis remains unknown. Purpose This study was designed investigate the PAT-derived high fat diet-induced obese rats. Methods results Hearts were isolated lean or Wistar rats for remodeling studies. Obese had abnormal structure, diastolic dysfunction, greatly elevated increased oxidative stress level. Enzyme-linked immunosorbent assay (ELISA) detected significantly higher than circulating level PAT obese, but not Western blot immunohistochemical analyses demonstrated receptor density heart. H9c2 rat cardiomyoblasts after exposed PAT-conditioned medium exhibited pronounced reactive oxygen species (ROS)-mediated apoptosis, which partially reversed by antagonist. Moreover, derived inhibited Na+/K+-ATPase activity cells through stimulating ROS, thereby activating calcium-dependent Pretreatment with specific inhibitors revealed that JAK2/STAT3 PI3K/Akt signaling pathways leptin-induced Conclusion induces via JAK2/STAT3/ROS pathway inhibiting downstream activity. FUNDunding Acknowledgement Type funding sources: Foundation. Main source(s): Nature Science Foundation ChinaKey Projects Shaanxi Technology Research Development Plan