Abstract
Perilla frutescens (L.) Britt. var. japonica (Hassk.) Hara (PF), is a medical herb of the Lamiaceae family. We have previously reported that the PF sprout extract (PFSE) is effective in treating hyperglycemia. However, the role of PFSE on glomerular mesangial cells (MCs) proliferation and the extracellular matrix (ECM) accumulation in a diabetic condition are still unclear. Therefore, in this study, we have investigated the role of PFSE on cell proliferation and ECM accumulation in murine glomerular MCs (MMCs), cultured under a high glucose (HG) condition. PFSE treatment attenuated HG-induced MMCs proliferation and hypertrophy. Moreover, the HG-induced ECM protein, collagen IV and fibronectin, overexpression was abolished by the PFFSE treatment. In addition, PFSE inhibited reactive oxygen species (ROS) overproduction and NOX2 and NOX4 expression in MMCs under a HG condition. Our data further revealed the involvement of mesangial cell damage in AMP-activated kinase (AMPK) activation. PFSE strongly activated AMPK in MMCs under hyperglycemic conditions. These results suggest that PFSE inhibits HG-medicated MC fibrosis through suppressing the activation of NOX2/4 and the AMPK activation mechanism. PFSE may be useful for the prevention or treatment of diabetic nephropathy.
Highlights
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease and is associated with increased mortality and morbidity [1]
PF sprout extract (PFSE) strongly activated AMPK in murine glomerular MCs (MMCs) under hyperglycemic conditions. These results suggest that PFSE inhibits high glucose (HG)-medicated mesangial cells (MCs) fibrosis through suppressing the activation of NOX2/4 and the AMPK activation mechanism
Since one of the earliest renal abnormalities observed after the onset of hyperglycemia often includes the proliferation of MCs, the PFSE was tested for its ability to inhibit MMCs proliferation in a HG (25 mmol/L) condition
Summary
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease and is associated with increased mortality and morbidity [1]. Glomerular mesangial cells (MCs) proliferation, hypertrophy, and ECM accumulation are hallmarks of diabetic nephropathy [2,3]. It has been known that ROS, at a low level, play an essential role in multiple cellular signal transduction pathways. Several studies support the finding that renal ROS play a central role in mediating renal injury in diabetes [4,5,6]. It has been reported that ROS play an important role in the pathogenesis of renal profibrotic factors in inducing fibroblast proliferation and/or activation [7]. Our previous studies confirmed that the ROS were increased in mesangial cells (MCs) in high-glucose conditions [8]. NADPH oxidases (NOX) are important sources of ROS involved in both normal physiological functions and oxidative stress [5]
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