Smooth Muscle Cells from a Rat Model of Obesity and Hyperleptinemia Are Partially Resistant to Leptin-Induced Reactive Oxygen Species Generation

• Published in: Antioxidants Vol. 12; no. 3; p. 728
• Main Authors: López-Acosta, Ocarol, Cristóbal-García, Magdalena, Cardoso-Saldaña, Guillermo, Carvajal-Aguilera, Karla, El-Hafidi, Mohammed
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.03.2023; MDPI
• Subjects: Abdomen; Animals; Aorta; Atherosclerosis; C cells; Cardiomyocytes; Cell culture; Coronary vessels; Genotype & phenotype; Glucose; Hypertension; Insulin; Leptin; metabolic syndrome and antioxidant defense; Muscle cells; Nitric oxide; Obesity; Oxidative stress; Phosphorylation; Physiological aspects; Plasma; Reactive oxygen species; Smooth muscle; smooth muscle cell; Stat3 protein; Sucrose; United States; United States > US; smooth muscle cell; leptin; metabolic syndrome and antioxidant defense; oxidative stress
• ISSN: 2076-3921; 2076-3921
• DOI: 10.3390/antiox12030728

The aim of this study was to evaluate the effect of leptin on reactive oxygen species' (ROS) generation of smooth muscle cells (SMCs) from a rat model of obesity and hyperleptinemia. Obesity and hyperleptinemia were induced in rats by a sucrose-based diet for 24 weeks. ROS generation was detected by using dichloro-dihydrofluorescein (DCF), a fluorescent ROS probe in primary SMCs culture. An increase in plasma leptin and oxidative stress markers was observed in sucrose-fed (SF) rats. At baseline SMCs from SF rats showed a more than twofold increase in fluorescence intensity (FI) compared to that obtained in control (C) cells. When the C cells were treated with 20 ng leptin, the FI increased by about 250%, whereas the leptin-induced FI in the SF cells increased only by 28%. In addition, sucrose feeding increased the levels of p22phox and gp91phox, subunits of Nox as an O source in SMCs. Treatment of cells with leptin significantly increased p22phox and gp91phox levels in C cells and did not affect SF cells. Regarding STAT3 phosphorylation and the content of PTP1B and SOCS3 as protein markers of leptin resistance, they were found to be significantly increased in SF cells. These results suggest that SF aortic SMCs are partially resistant to leptin-induced ROS generation.