Praveen Kumar Issac1, Manikandan Velayutham2, Ajay Guru2, Gokul Sudhakaran2, Raman Pachaiappan3, Jesu Arockiaraj4,5. 1. Institute of Biotechnology, Saveetha School of Engineering, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, 602 105, India. 2. Department of Biotechnology, College of Science and Humanities, SRM Institute of Science and Technology, Kattankulathur, Chennai, Tamil Nadu, 603 203, India. 3. Department of Biotechnology, School of Bioengineering, College of Engineering and Technology, SRM Institute of Science and Technology, Kattankulathur, Chennai, Tamil Nadu, 603 203, India. 4. Department of Biotechnology, College of Science and Humanities, SRM Institute of Science and Technology, Kattankulathur, Chennai, Tamil Nadu, 603 203, India. jesuaraj@hotmail.com. 5. Foundation for Aquaculture Innovations and Technology Transfer (FAITT), Thoraipakkam, Chennai, Tamil Nadu, 600 097, India. jesuaraj@hotmail.com.
Abstract
BACKGROUND: The development of diabetic nephropathy is aided by the presence of oxidative stress. Morin, a natural flavonoid molecule, has been shown to have antioxidant and anti-diabetic properties. However, little is known about the mechanism of its protective effect in diabetic nephropathy pathogenesis caused by oxidative stress. METHODS: Using Madin-Darby canine kidney (MDCK) cells as a working model, the current study investigates the detailed mechanism of morin's beneficial action. In hydrogen peroxide-induced oxidative stressed MDCK cells, there was a considerable rise in intracellular ROS and decreased antioxidant enzyme levels. RESULTS: Morin has a higher binding affinity for the antioxidant receptor; according to in silico study using molecular docking and ADMET, it is predicted to be an orally active molecule. While morin administration increased SOD and CAT activity in oxidative stress-induced MDCK cells, it also reduced mitochondrial oxidative stress and apoptosis. Furthermore, the present study discovered the molecular mechanism through which morin reduced oxidative stress in MDCK cells by upregulating antioxidant enzyme molecules including GST, GPx, and GCS. CONCLUSION: These findings suggest that morin reduces H2O2-induced oxidative stress, reduces DNA oxidative damage, and prevents the depletion of antioxidant genes in MDCK cells.
BACKGROUND: The development of diabetic nephropathy is aided by the presence of oxidative stress. Morin, a natural flavonoid molecule, has been shown to have antioxidant and anti-diabetic properties. However, little is known about the mechanism of its protective effect in diabetic nephropathy pathogenesis caused by oxidative stress. METHODS: Using Madin-Darby canine kidney (MDCK) cells as a working model, the current study investigates the detailed mechanism of morin's beneficial action. In hydrogen peroxide-induced oxidative stressed MDCK cells, there was a considerable rise in intracellular ROS and decreased antioxidant enzyme levels. RESULTS: Morin has a higher binding affinity for the antioxidant receptor; according to in silico study using molecular docking and ADMET, it is predicted to be an orally active molecule. While morin administration increased SOD and CAT activity in oxidative stress-induced MDCK cells, it also reduced mitochondrial oxidative stress and apoptosis. Furthermore, the present study discovered the molecular mechanism through which morin reduced oxidative stress in MDCK cells by upregulating antioxidant enzyme molecules including GST, GPx, and GCS. CONCLUSION: These findings suggest that morin reduces H2O2-induced oxidative stress, reduces DNA oxidative damage, and prevents the depletion of antioxidant genes in MDCK cells.
Authors: A Ceriello; N Bortolotti; E Falleti; C Taboga; L Tonutti; A Crescentini; E Motz; S Lizzio; A Russo; E Bartoli Journal: Diabetes Care Date: 1997-02 Impact factor: 19.112
Authors: Ajay Guru; Christy Lite; Allen J Freddy; Praveen Kumar Issac; Mukesh Pasupuleti; N T Saraswathi; Mariadhas Valan Arasu; Naif Abdullah Al-Dhabi; Aziz Arshad; Jesu Arockiaraj Journal: Dev Comp Immunol Date: 2020-09-10 Impact factor: 3.636