Effect of Aspirin on the Expression of Hepatocyte NF-kappaB and Serum TNF-alpha in Streptozotocin-Induced Type 2 Diabetic Rats.
10.3346/jkms.2011.26.6.765
- Author:
Xiaodong SUN
1
;
Fang HAN
;
Junling YI
;
Lina HAN
;
Ben WANG
Author Information
1. Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China. sxdfriend@sina.com
- Publication Type:Original Article
- Keywords:
Inflammation;
Insulin Resistance;
Aspirin
- MeSH:
Animals;
Anti-Inflammatory Agents, Non-Steroidal/*pharmacology;
Aspirin/*pharmacology;
Blood Glucose/analysis;
Diabetes Mellitus, Experimental/blood/chemically induced/*metabolism;
Fatty Acids, Nonesterified/blood;
Hypoglycemic Agents/*pharmacology;
Insulin/blood;
Insulin Resistance;
Liver/metabolism;
Male;
Metformin/therapeutic use;
NF-kappa B/*metabolism;
Rats;
Rats, Wistar;
Tumor Necrosis Factor-alpha/*blood
- From:Journal of Korean Medical Science
2011;26(6):765-770
- CountryRepublic of Korea
- Language:English
-
Abstract:
Aspirin is a kind of anti-inflammatory drug and may be used to reverse hyperglycemia, hyperinsulinemia, and dyslipidemia by improving insulin resistance. We hypothesized that aspirin improves insulin resistance in type 2 diabetes by inhibiting hepatic nuclear factor kappa-beta (NF-kappaB) activation and serum tumor necrosis factor-alpha (TNF-alpha). Adult male Wistar rats were randomly divided into four groups: control, untreated diabetic, diabetic treated with metformin (100 mg/kg/day), and diabetic treated with aspirin (120 mg/kg/day). Diabetes was induced by high-fat feeding and a low dose of streptozotocin (30 mg/kg). After treatment, plasma glucose, insulin, lipids, free fatty acids (FFAs) concentrations and serum TNF-alpha were determined. The expression of NF-kappaB in hepatocytes was analyzed by immunohistochemistry and western blot. The results showed administration of aspirin caused no significant lowering in fasting glucose level but significant reduction of hepatic NF-kappaB expression and serum TNF-alpha level with improved insulin resistance compared to the diabetic group. The relevant analysis showed positive correlation between the expression of homeostasis model assessment-insulin resistance (HOMA-IR) and NF-kappaB (r = 0.799, P < 0.01); HOMA-IR and serum TNF-alpha (r = 0.790, P < 0.01). It is concluded that aspirin improves insulin resistance by inhibiting hepatic NF-kappaB activation and TNF-alpha level in streptozotocin-induced type 2 diabetic rats.
