Rosemarinic acid protects β-cell from STZ-induced cell damage via modulating NF-κβ pathway
Waseem El-Huneidi,
Shabana Anjum,
Abdul Khader Mohammed,
Shuhd Bin Eshaq,
Sham Abdrabh,
Yasser Bustanji,
Nelson C. Soares,
Mohammad H. Semreen,
Karem H. Alzoubi,
Eman Abu-Gharbieh,
Jalal Taneera
Affiliations
Waseem El-Huneidi
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; College of Medicine, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; Corresponding author. Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates.
Shabana Anjum
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; College of Engineering, Drug Delivery Research Group, American University of Sharjah, Sharjah, United Arab Emirates
Abdul Khader Mohammed
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates
Shuhd Bin Eshaq
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates
Sham Abdrabh
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates
Yasser Bustanji
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; College of Medicine, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; School of Pharmacy, The University of Jordan, Amman, 11942, Jordan
Nelson C. Soares
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; College of Pharmacy, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; Department of Human Genetics, National Institute of Health Doutor Ricardo Jorge (INSA), Lisbon, Portugal
Mohammad H. Semreen
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; College of Pharmacy, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates
Karem H. Alzoubi
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; College of Pharmacy, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates
Eman Abu-Gharbieh
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; College of Medicine, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates
Jalal Taneera
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; College of Medicine, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates; Corresponding author. Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, P.O. Box 27272, United Arab Emirates.
Rosmarinic acid (RA), a natural ester phenolic compound, is known to have antioxidant and anti-inflammatory properties. RA has also been reported to exhibit a hypoglycemic effect; however, the mechanisms underlying this effect have yet to be investigated. Therefore, the present study focused on the anti-diabetic effects and mechanism of RA in INS-1 cells using in vitro model. Streptozotocin (STZ) at a concentration of 3 mM was applied to INS-1 cells for 4 h to create a diabetic model. The cells were pretreated for 24 h with various concentrations (1 and 2.5 μM) of RA. The Cell viability, glucose-stimulated insulin secretion (GSIS), glucose uptake, lipid peroxidation, reactive oxygen species (ROS), apoptosis, and protein expression of Bcl-2, NF-κB, 1L-1β, and PARP were assessed. Results showed that STZ-treated INS-1 cells exhibited reduced cell viability, insulin release, insulin content, glucose uptake, and elevated MDA and ROS levels. Cells pretreated with RA maintained the function and morphology of β-cells against STZ-induced damage. Moreover, RA sustained high protein expression levels of Bcl-2 and low expression levels of NF-κB, IL-1β, and PARP. In conclusion, RA preserved β-cells function against STZ-induced damage by altering NF-κB and Bcl-2 pathways.
