RÉSUMÉ
Objective To observe the effect of rosiglitazone on the protein expression of AMPK and GLUT4 in peripheral tissue (liver, skeletal muscle and fat) of type 2 diabetic db/db mice and to prove that rosiglitazone can regulate the glucose metabolism in db/db mice partly through the AMPK pathway. Methods db/db mice were randomly divided into model group and rosiglitazone group according to their blood glucose.The db/m mice were normal control group.After 4 weeks of administration, fasting blood glucose was detected in each group.Western blot was used to detect the contents of AMPK, p-AMPK and GLUT4 in liver, skeletal muscle and adipose tissue. Results (1) Rosiglitazone significantly reduced the fasting blood glucose of db/db mice; (2)Rosiglitazone increased the level of AMPK phosphorylation in the liver, skeletal muscle and adipose tissue of db/db mice, and increased the content of GLUT4 protein in skeletal muscle and adipose tissue. Conclusion Rosiglitazone can increase the phosphorylation of AMPK and the expression of GLUT4 protein in the liver, muscle and fat tissue of db/db mice, and promote the uptake and utilization of glucose in peripheral tissue, suggesting that it can regulate glucose metabolism in db/db mice partly through the AMPK pathway.
RÉSUMÉ
Diabetic retinopathy (DR) is an important cause of vision loss and blindness in diabetic patients. Studies have shown that neurodegenerative changes have occurred before diabetic retinal microvascular injury, such as reactive glial increase and ganglion cell apoptosis, and endoplasmic reticulum stress is involved in this process.Studies have shown that neurodegenerative changes have occurred before diabetic retinal microvascular injury, mainly as ganglion cell apoptosis, and endoplasmic reticulum stress is involved in this process.The UPR has three signal paths:the ATF6 signal path, the PERK signal path, and the IRE1 signal path.It is closely related to oxidative stress, inflammation, apoptosis, BRB destruction and angiogenesis in the DR process.Exploring the intrinsic mechanism of ERS and ganglion cell injury is of great significance for finding new effective drugs to prevent or treat diabetic patients.