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• W4292749483 abstract "<ns4:p><ns4:bold>Introduction: </ns4:bold>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.</ns4:p><ns4:p> <ns4:bold>Methods:</ns4:bold> 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.</ns4:p><ns4:p> <ns4:bold>Results:</ns4:bold> 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).</ns4:p><ns4:p> <ns4:bold>Conclusions:</ns4:bold> DBLS3233 significantly reduces the inflammatory process and enhances the expression of GLUT1 and GLUT2 diabetic rats.</ns4:p>" @default.
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• W4292749483 date "2022-08-23" @default.
• W4292749483 modified "2023-10-16" @default.
• W4292749483 title "DLBS3233 reduces inflammatory marker on kidney by increasing expression GLUT1 and GLUT2 in diabetic rats" @default.
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• W4292749483 doi "https://doi.org/10.12688/f1000research.123091.1" @default.
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