Sahar Koushki
1, Reza Mohammadrezaei Khorramabadi
1, Peyman Amanolahi Baharvand
2, Amin Hasanvad
3* 
1 Student Research Committee, Lorestan University of Medical Sciences, Khorramabad, Iran
2 Razi Herbal Medicines Research Center, Lorestan University of Medical Sciences, Khorramabad, Iran
3 Nutritional Health Research Center, Department of Pharmacology and ،oxicology, Faculty of Pharmacy, Lorestan University of Medical Sciences, Khorramabad, Iran
Abstract
The mechanism of metformin includes the enhancement of skeletal muscles and adipocytes glucose uptake,
and inhibiting the production of glucose in liver. AMP-activated protein kinase (AMPK) via metformin,
a cellular energy regulator, can be used to balance hemostasis. Treatment with metformin in glomerular
mesangial cells (MCs) in a diabetic situation has resulted in the significant increase of superoxide dismutase
(SOD) and malondialdehyde (MDA), monocyte chemoattractant protein-1 (MCP-1), p38 mitogen-activated
protein kinase (p38MAPK) expression, the expression of nuclear factor-κB (NF-κB), intracellular p22phox
mRNA and protein level, intercellular adhesion molecule-1 (ICAM-1), proinflammatory cytokines,
transforming growth factor-beta 1 (TGF-β1) and ROS production suppression and lipid peroxidation.
Metformin also has a reno-protective mechanism, i.e., restoring mitochondrial function integrity.