Abstract
This study aims to investigate the wound-healing effectiveness of the phenolic compound, naringin, both in vitro and in vivo. Male mice were shaved on their dorsal skin under isoflurane, a biopsy punch was made in four symmetrical circular resection windows (6 mm) to induce a wound. These excision wounds were used to study the topical effects of naringin in terms of various biochemical, molecular, and histological parameters. We observed a significant recovery in the wound area. Increased levels of MMP-2, 9, 14, TIMP-2, VEGF-A, and VEGF-R1 were induced by naringin in the HaCaT cells. The time course experiments further revealed that levels of VEGF-A and B increased within 36 h; whereas levels of VEGF-C decreased. In line with this, VEGF-R3 levels, but not VEGF-R1 and 2 levels, increased soon after stimulation; although the increase subsided after 36 h. Additionally, naringin cream upregulated wound healing in vitro. The blockage of VEGF by Bevacizumab abolished the function of naringin cream on cell migration. Histological alterations in the wounded skin were restored by naringin cream, which accelerated wound healing via upregulated expression of growth factors (VEGF-A, B, and C and VEGF-R3), and thus increased MMP-2, 9, 14 expressions.
Highlights
The healing of a skin wound presents a complex process involving a cascade of cellular functions
The blockage of VEGF-mediated MMP activation by bevacizumab abolished or perturbed the function of naringin in the wound healing assay and migration in vitro. These findings suggest that activation of the VEGF signaling pathway and relatively higher expressions of MMP-2 and 9 may contribute to the function of naringin serving as a prognostic initiator in wound healing
The current study demonstrates the effectiveness of naringin to accelerate and enhance the wound-healing process via several mechanisms
Summary
The healing of a skin wound presents a complex process involving a cascade of cellular functions. The wound repair process commonly leads to the substitution of the superficial epidermis, mucosa, or fetal skin, and skin repair displays an unspecific form of healing, wherein the wound is healed by a non-functional mass of fibrotic tissue known as scar tissue [1–4]. Wounds can take longer to heal in patients with diabetes, resulting in increased risks of infection and of developing dangerous symptoms [6–8]. Chronic wounds fail to heal by not following a predictable or expected healing pathway. The care of chronic wounds has evolved into its own specialty, with physicians often using a variety of therapies, including engineered skin, growth factors, pressure wound therapy (NPWT), and negative extracellular matrices (ECMs) [9]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
