Modulation of the Oxidative Stress and ICAM-1/TLR4/NF-Κβ Levels by Metformin in Intestinal Ischemia/Reperfusion...

Area of Science:

• Pharmacology
• Gastroenterology
• Pathophysiology

Background:

• Intestinal ischemia-reperfusion (I/R) injury is a serious clinical condition.
• Metformin, an antihyperglycemic agent, has shown potential anti-inflammatory properties.

Purpose of the Study:

• To investigate the protective effects of metformin against experimental intestinal I/R injury.
• To evaluate metformin's impact on oxidative stress and inflammatory markers in I/R.

Main Methods:

• Rats underwent superior mesenteric artery occlusion followed by reperfusion to induce I/R injury.
• Metformin was administered orally at varying doses (50, 100, 200 mg/kg) for one week prior to surgery.
• Tissue analysis included malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity, ICAM-1, TLR4, NF-κB, and histopathology.

Main Results:

• Metformin reduced MDA levels at 100 and 200 mg/kg.
• MPO activity and ICAM-1 levels were decreased by metformin at all tested doses.
• NF-κB levels were reduced at 200 mg/kg, and histopathological scores improved at 100 and 200 mg/kg.

Conclusions:

• Metformin demonstrates protective effects against I/R-induced intestinal injury.
• The mechanism involves down-regulation of ICAM-1 and NF-κB, reduced oxidative stress, and decreased neutrophil infiltration.
• Metformin is a potential therapeutic agent for managing intestinal I/R injury.