Folic Acid (FA) induced Renal Fibrosis Modeling & Pharmacodynamics Service

Creative Biolabs offers a range of well-established models to evaluate drug efficacy in Chronic Kidney Disease. These models provide valuable tools for researchers developing new therapies aimed at slowing disease progression and improving kidney function.

Introduction

Chronic Kidney Disease (CKD) is a progressive condition characterized by a gradual decline in kidney function over a period of months or years. It affects millions of people worldwide and is a major cause of morbidity and mortality. The disease is commonly caused by underlying conditions such as diabetes, hypertension, and glomerulonephritis, among others. As kidney function deteriorates, the ability to filter waste products from the blood decreases, leading to an accumulation of harmful substances. Symptoms of CKD include fatigue, fluid retention, high blood pressure, and abnormal urine output. If left untreated, CKD can progress to end-stage renal disease (ESRD), requiring dialysis or a kidney transplant. Early detection and intervention are critical to slowing the progression of the disease and improving patient outcomes.

Folic acid (FA)-Induced Renal Fibrosis Model

The Folic Acid-Induced Renal Fibrosis Model involves the administration of folic acid (FA) to rodents, leading to the development of renal fibrosis. The method includes the injection of FA, which induces nephropathy by causing inflammation, tubular injury, and fibrosis in the kidneys. Key advantages of this model include its reproducibility and ability to reflect the fibrotic stages of renal disease, making it ideal for testing interventions aimed at halting fibrosis progression. However, one limitation is that the model may not fully replicate all human CKD phenotypes, particularly in terms of metabolic comorbidities.

  • Simulates: The FA-induced renal fibrosis model simulates chronic kidney disease (CKD), specifically focusing on the fibrotic progression in kidney tissues.
  • Evaluates Drugs: It is ideal for assessing the effects of anti-fibrotic drugs, anti-inflammatory agents, and renoprotective therapies aimed at mitigating kidney damage and slowing the progression of CKD.

Evaluation Platform

  • Animals: Mouse, Rat.
  • Measurements
    We offer a range of assessments for evaluating drug efficacy in the Folic Acid-Induced Renal Fibrosis Model, using advanced technologies such as:
    • General observations: body weight, mortality rate, and urine output.
    • Histopathological evaluation: kidney tissue examination for fibrosis, tubular atrophy, and glomerulosclerosis.
    • Immunohistochemistry: quantification of immune cell infiltration (e.g., macrophages, T-cells) and fibrosis markers (e.g., collagen, α-SMA).
    • Biomarker analysis: serum creatinine, blood urea nitrogen (BUN), and urinary protein levels.
    • Gene/protein expression profiling: via RT-qPCR and Western blot for fibrosis-related genes (e.g., TGF-β, CTGF).

In addition to these established methods, we can develop novel biomarker panels tailored to specific research needs, and our team is available for comprehensive support throughout experimental design, data collection, and analysis.

Related Services

We provide services for other CKD models. These models are particularly useful for testing therapies aimed at different stages of kidney disease progression, providing a more comprehensive assessment of drug efficacy.

Our advantages

  • Comprehensive expertise: We offer in-depth knowledge of CKD models, providing accurate and reproducible results.
  • Tailored solutions: Customizable experimental designs based on specific research needs.
  • Advanced technologies: State-of-the-art techniques for monitoring disease progression and evaluating drug efficacy.
  • Scientific support: Our team of experts provides assistance in experimental planning, data analysis, and interpretation of results.
  • Fast turnaround: Efficient processing and reporting to accelerate your research timelines.

Work with Us

1
Inquiry Stage
  • Summarize the project requirements and fill in the information collection form.
  • Sign a CDA from both parties to further communicate information, such as targets.
  • Select an animal model, discuss experimental design, and determine assay parameters.
  • Project costing and project schedule forecasting.
2
Project Start
  • We provide a detailed project plan, including the required sample quantities, methods, and protocols.
  • Both parties confirm the project details and start the project.
  • Confirm the timeline of the project.
3
Project Progress
  • We provide periodic results and information on the animal's condition.
  • We will work together to make project adjustments as necessary.
4
Project Completion
  • We provide a comprehensive project report promptly.
  • We arrange transportation for the produced samples.
  • We provide a discussion of the project results and help to arrange the next steps.
5
After-Sales Support
  • Data storage and archiving.

Get in touch!

FAQs

  1. 1. What are the key advantages of the Folic Acid-Induced Renal Fibrosis Model?

    This model closely mimics the development of kidney fibrosis in CKD, allowing for the assessment of anti-fibrotic therapies and drug interventions. It’s especially useful for testing drugs that target inflammation and fibrosis.

  2. 2. Can this model be used to evaluate both acute and chronic kidney injury?

    The Folic Acid-Induced Renal Fibrosis Model primarily focuses on chronic kidney injury and fibrosis, but it can provide insights into the progression from acute to chronic stages of kidney damage.

  3. 3. How long does it take to develop kidney fibrosis in this model?

    Renal fibrosis typically begins to develop within 2-3 weeks after folic acid administration, with significant fibrosis observed within 4-6 weeks.

  4. 4. What kind of support do you provide during the experiment?

    We offer full scientific and technical support throughout the process, including experimental design, protocol development, data collection, and analysis.

  5. 5. Is this model suitable for evaluating drug combinations?

    Yes, this model can be used to test single-drug or combination therapies aimed at preventing or reversing renal fibrosis.

Published Data

ILK deficiency prevents FA-induced renal fibrosis. (OA Literature) Fig. 1 FA-induced renal fibrosis is prevented by the lack of ILK.1

The study employed a renal damage model induced by folic acid (FA) on transgenic mice and cultured human tubular epithelial cells (HK2) with ILK depletion. Figure 1 presents the analysis of extracellular matrix (ECM) proteins, fibronectin (FN), and collagen type 1 (COL1A1), in renal samples from various experimental groups. In wild-type (WT) FA-treated mice, the expressions of FN (Figure 1A) and COL1A1 (Figure 1B) were significantly increased compared to the WT control (CT) group. However, this upregulation was prevented in the cKD-ILK FA group. Histopathological analysis of ECM deposition was conducted on kidney sections following FA treatment using Sirius red staining, and the red intensity per area was measured. As shown in Figure 1C, WT FA mice displayed higher interstitial red staining, indicating increased collagen deposition, in contrast to the WT CT group. This increase in collagen deposition was effectively blocked in the cKD-ILK FA group.

Reference

  1. de la Serna-Soto, Mariano et al. "Integrin-Linked Kinase (ILK) Promotes Mitochondrial Dysfunction by Decreasing CPT1A Expression in a Folic Acid-Based Model of Kidney Disease." International Journal of Molecular Sciences vol. 26,5 1861. 21 Feb. 2025. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.3390/ijms26051861

For Research Use Only.


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