Abstract
Introduction: Diabetic kidney disease (DKD), as a diabetes mellitus type 2 (DMT2) complications, is getting more prevalent nowadays. Inflammation is one of the renal injury mechanisms evaluated through the surge in in TNF-α and NF-κβ expression. Impaired expression of gluten transporter 1 (GLUT1) and GLUT2 reduces glucose uptake. DBLS3233 is a novel anti-diabetes agent and Indonesian herbal product responsible for glucose control and upregulation of insulin signal transduction. We performed an experiment on DLBS3233 to examine the response of TNF-α and NF-κβ and the expression of GLUT 1 and GLUT2. Methods: A total of 30 adult male Wistar rats were randomly divided into six groups (n=5 per group): nondiabetic rats in the control group (group 1); untreated diabetic rats (group 2); diabetic rats treated with DLBS3233 4,5mg/kgBW (group 3); 9mg/kgBW (group 4); 18mg/kgBW (group 5), and diabetic rats treated with pioglitazone (group 6). Immunohistochemistry was performed to examine the expression of GLUT1 and GLUT2 in the pancreas and expression of TNF-α and NF-κβ in the kidney. The data was then analyzed by ANOVA. Results: In the DBLS3233 group, reduced expression of both TNF-α and NF-κβ was seen through immunohistochemistry, whereas GLUT1 and GLUT2 were intensified compared to untreated groups. From statistical analysis, we obtained significantly lower expression of TNF-α and NF-κβ, as well as enhanced GLUT1 and GLUT2 expression compared to untreated groups (p<0.05). Conclusions: DBLS3233 significantly reduces the inflammatory process and enhances the expression of GLUT1 and GLUT2 diabetic rats.
Subject
General Pharmacology, Toxicology and Pharmaceutics,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine
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1 articles.
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