Unraveling the Inflammatory Symphony: Dissecting the Dysregulated Nf-Κb, Il-6, and Ifn-Γ in Nephropathy Patients Publisher



Jabbari N¹ ; Gheibi P² ; Makki YB² ; Azizi Z³ Show Affiliations
Source: Journal of Bioscience and Applied Research Published:2024

Abstract

Background: Diabetes patients have been known to activate the inflammasome pathway. The current research was carried out to assess the gene expression levels of nuclear factor-κappa B (NF-κB), Interleukin 6 (IL-6), and Interferon Gamma (IFN-γ) in PBMC samples from peripheral blood to find out whether its mRNA could be used as an early marker for renal function deterioration in diabetics. Methods: This empirical study collected serum samples from 60 diabetic patients suffering from nephropathy and 60 healthy controls. Collected blood from the patients was isolated and preserved in the medium at a temperature of-20. Fasting blood sugar (FBS), total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, cholesterol/HDL-LDL, AST, ALT, alkaline phosphatase, and CBC were analyzed. Real-time PCR measured NF-κB, IL-6, and IFN-γ gene expression. Results: Diabetic patients with nephropathy showed increased fasting plasma glucose levels compared to non-diabetic subjects, although there were no significant differences between them regarding cholesterol, triglyceride or other lipid levels, white blood cell count, and red blood cell count. Along with platelet count parameters, the levels of MCV, MCH, MCHC, RDW-CV, AST, ALT, and alkaline phosphatase did not change in the control group. The patient group showed a significant increase in NF-κB and IL-6 gene expression at the level of (P-value <0.001) and also IFN-γ expression at the level of (P-value <0.01) compared to the healthy control group. Conclusion: Due to the elevated level of these genes in nephropathic patients, it can be possibly concluded that NF-κB, IL-6, and IFN-γ are involved in nephropathy complications of diabetes. © 2024, Society of Pathological Biochemistry and Hematology. All rights reserved.