Related Experiment Video
Updated: May 1, 2026
Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
Published on: May 10, 2024
Glibenclamide treatment modulates the expression and localization of myosin-IIB in diabetic rat brain
Alice Vieira da Costa1, Luciana Karen Calábria2, Paula de Souza Santos1
1Institute of Genetics and Biochemistry, Federal University of Uberlândia, Campus Umuarama, Uberlândia, MG 38400-902, Brazil.
Background:
Myosin-IIB is a non-muscle isoform in the brain with increased expression in the brains of diabetic rats. Chronic hyperglycemia caused by diabetes can impair learning and memory. Oral hypoglycemic agents such as glibenclamide have been used to control hyperglycemia. We report changes in the expression and distribution of myosin-IIB in the frontal cortex and hippocampus of diabetic rats treated with glibenclamide.
Methods:
The brains were removed after 43 days of treatment with glibenclamide (6 mg/kg bw orally), homogenized and analyzed by Western blotting, qRT-PCR and immunohistochemistry.
Results:
Myosin-IIB expression increased in the brains of diabetic rats. However, protein expression returned to control levels when treated with glibenclamide. In addition, the expression of MYH10 gene encoding non-muscle myosin heavy chain-B decreased in diabetic rats treated with glibenclamide. Moreover, we found weak myosin-IIB labeling in the hippocampus and frontal cortex of rats treated with glibenclamide. Therefore, the expression of myosin-IIB is affected by diabetes mellitus and may be modulated by glibenclamide treatment in rats. Structural changes in the hippocampus and prefrontal cortex are reversible, and glibenclamide treatment may reduce the patho-physiological changes in the brain.
Conclusions:
Our findings can contribute to the understanding of the regulation of myosins in the brains of diabetic rats.
More Related Videos
Related Concept Videos
01:23Dipeptidyl Peptidase 4 Inhibitors
01:06Oral Hypoglycemic Agents: Glinides
01:24Glucagon-like Receptor Agonists
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...