Title:Effect of Bovine Lactoferrin Treatment on Iron Homeostasis and Gene
Expression Changes in Multiple Organ Dysfunctions During Wound
Healing Process in Rats
Volume: 24
Issue: 5
Author(s): Ahmet Sarper Bozkurt*Şenay Görücü Yılmaz
Affiliation:
- Department of Physiology, Faculty of Medicine, University of Gaziantep, Gaziantep, Turkey
Keywords:
Bovine lactoferrin, wound healing, PHGPx, SLC7A11, SLC40A1, FSTD.
Abstract:
Background: Injury systemically disrupts the homeostatic balance and can cause organ
failure. LF mediates both iron-dependent and iron-independent mechanisms, and the role of LF in
regulating iron homeostasis is vital in terms of metabolism.
Objectives: In this study, we evaluated the organ-level effect and gene expression change of bLf
in the cutaneous repair process.
Materials and Methods: An excisional full-thickness skin defect (FTSD) wound model was created
in male Sprague Dawley rats (180-250 g) (n = 48) fed a high-fat diet (HFD) and the PHGPx,
SLC7A11 and SLC40A1 genes and iron metabolism were evaluated. The animals were randomly
divided into 6 groups: 1- Control, 2- bLf (200 mg/kg/day, oral), 3- FTSD (12 mm in diameter, dorsal),
4- HFD + bLf, 5- HFD + FTSD, 6- HFD + FTSD + bLf. Histologically, iron accumulation
was demonstrated by Prussian blue staining in the liver, kidney, and intestinal tissues. Gene expression
analysis was performed with qPCR.
Results: Histologically, iron accumulation was demonstrated by Prussian blue staining in the liver,
kidney, and intestinal tissues. Prussian blue reactions were detected in the kidney. PHPGx and
SLC7A11 genes in kidney and liver tissue were statistically significant (P < 0.05) except for the
SLC40A1 gene (P > 0.05). Expression changes of the three genes were not statistically significant
in analyses of rat intestinal tissue (P = 0.057).
Conclusion: In the organ-level ferroptotic damage mechanism triggered by wound formation. BLf
controls the expression of three genes and manages iron deposition in these three tissues. In addition,
it suppressed the increase in iron that would drive the cell to ferroptosis and anemia caused
by inflammation, thereby eliminating iron deposition in the tissues.