Related Experiment Video
Updated: Jan 29, 2026

Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
Macrophage migration inhibitory factor antagonist (p425) ameliorates kidney histopathological and functional changes
Jamal Khalilpour1, Shiva Roshan-Milani1,2, Farzaneh Hosseini Gharalari3,4
1Urmia University of Medical Sciences, Department of Physiology, Faculty of Medicine, Urmia, Iran.
Introduction:
It is hypothesized that increased macrophage migration inhibitory factor (MIF) expression may contribute to diabetic nephropathy (DN) pathogenesis. The aim of the present study was to investigate the renal effects of MIF inhibition in a diabetic experimental model.
Methods:
Eighteen male Wistar rats (230 ± 20 g) were divided into three groups: 1) control, 2) diabetic (STZ, 50 mg/kg, dissolved in saline, ip), 3) diabetic + MIF antagonist (p425, 1 mg/kg per day, ip, on the 21th day, for 21 consecutive days). The treatment started since we founwd a significant increase in urine albumin excretion (UAE) rate in the diabetic rats in comparison with the control rats. The rats were kept individually in metabolic cages (8 AM-2 PM) and urine samples were collected in the 21 and 42th day. At the end, blood and tissue samples were collected for biochemical (BS, UPE, urine GAG, BUN, Cr, Na, and K) and histological analyses.
Results:
The results of this study showed that MIF antagonist (p425) significantly decreased urine protein and GAG excretion, urine protein/creatinine ratio, and serum BUN and Cr in the streptozotocin-induced DN in the rats. Pathological changes were significantly alleviated in the MIF antagonist (p425)-administered DN rats.
Conclusion:
Collectively, these data suggested that MIF antagonist (p425) was able to protect against functional and histopathological injury in the DN.
Insights
Inhibition of macrophage migration inhibitory factor (MIF) protected against diabetic nephropathy (DN) in rats. MIF antagonist treatment reduced kidney damage and improved renal function in a diabetic model.
Area of Science:
- Nephrology
- Immunology
- Endocrinology
Background:
- Macrophage migration inhibitory factor (MIF) is implicated in diabetic nephropathy (DN) pathogenesis.
- Investigating MIF's role in DN is crucial for understanding disease mechanisms.
Purpose of the Study:
- To evaluate the therapeutic potential of MIF inhibition in a rat model of DN.
- To assess the renal effects of a specific MIF antagonist (p425) in diabetic conditions.
Main Methods:
- Streptozotocin-induced diabetic Wistar rats were treated with MIF antagonist (p425).
- Urine albumin excretion, biochemical markers (BUN, Cr), and histological changes were analyzed.
- Treatment commenced upon observing increased urine albumin excretion in diabetic rats.
Main Results:
- MIF antagonist (p425) significantly reduced urine protein and GAG excretion.
- Treatment lowered urine protein/creatinine ratio and serum BUN and creatinine levels.
- Histopathological analysis revealed significant alleviation of kidney damage in treated rats.
Conclusions:
- MIF antagonist (p425) demonstrates protective effects against functional and histopathological kidney injury in DN.
- Targeting MIF presents a potential therapeutic strategy for managing diabetic nephropathy.
More Related Videos
Related Concept Videos
Kidney Structure
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
Transcription Factors
Cholinergic Antagonists: Pharmacokinetics
Excitatory and Inhibitory Effects of Neurotransmitters
Migration

