Wound healing and anti-inflammatory activities of bee venom-chitosan blend films

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inﬂammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inﬂammation responses.

Download Full-text

In vitro anti-inflammatory and wound healing activities of Citrus auraptene

Planta Medica ◽

10.1055/s-0032-1320270 ◽

2012 ◽

Vol 78 (11) ◽

Author(s):

F Epifano ◽

S Genovese ◽

L Zhao ◽

V Dang La ◽

D Grenier

Keyword(s):

Wound Healing ◽

Anti Inflammatory

Download Full-text

Azadirachta indica A. Juss (Neem) oil topical formulation with liquid crystals ensconcing depot water for anti-inflammatory, wound healing and anti-methicillin resistant Staphylococcus aureus activities

Journal of Drug Delivery Science and Technology ◽

10.1016/j.jddst.2021.102563 ◽

2021 ◽

pp. 102563

Author(s):

Kaushita Banerjee ◽

Monami Chatterjee ◽

Rajendra Sandur V ◽

Ramesh Nachimuthu ◽

Harishkumar Madhyastha ◽

...

Keyword(s):

Staphylococcus Aureus ◽

Wound Healing ◽

Liquid Crystals ◽

Azadirachta Indica ◽

Methicillin Resistant Staphylococcus Aureus ◽

Neem Oil ◽

Topical Formulation ◽

Methicillin Resistant ◽

Anti Inflammatory

Download Full-text

Inflammatory M1-like macrophages polarized by NK-4 undergo enhanced phenotypic switching to an anti-inflammatory M2-like phenotype upon co-culture with apoptotic cells

Journal of Inflammation ◽

10.1186/s12950-020-00267-z ◽

2021 ◽

Vol 18 (1) ◽

Author(s):

Keizo Kohno ◽

Satomi Koya-Miyata ◽

Akira Harashima ◽

Takahiko Tsukuda ◽

Masataka Katakami ◽

...

Keyword(s):

Wound Healing ◽

Chronic Wounds ◽

Macrophage Polarization ◽

Phenotypic Switching ◽

Apoptotic Cells ◽

Phenotypic Switch ◽

Inflammatory Phase ◽

M1 Macrophage ◽

Tnf Α ◽

Anti Inflammatory

Abstract Background NK-4 has been used to promote wound healing since the early-1950s; however, the mechanism of action of NK-4 is unknown. In this study, we examined whether NK-4 exerts a regulatory effect on macrophages, which play multiple roles during wound healing from the initial inflammatory phase until the tissue regeneration phase. Results NK-4 treatment of THP-1 macrophages induced morphological features characteristic of classically-activated M1 macrophages, an inflammatory cytokine profile, and increased expression of the M1 macrophage-associated molecules CD38 and CD86. Interestingly, NK-4 augmented TNF-α production by THP-1 macrophages in combination with LPS, Pam3CSK4, or poly(I:C). Furthermore, NK-4 treatment enhanced THP-1 macrophage phagocytosis of latex beads. These results indicate that NK-4 drives macrophage polarization toward an inflammatory M1-like phenotype with increased phagocytic activity. Efferocytosis is a crucial event for resolution of the inflammatory phase in wound healing. NK-4-treated THP-1 macrophages co-cultured with apoptotic Jurkat E6.1 (Apo-J) cells switched from an M1-like phenotype to an M2-like phenotype, as seen in the inverted ratio of TNF-α to IL-10 produced in response to LPS. We identified two separate mechanisms that are involved in this phenotypic switch. First, recognition of phosphatidylserine molecules on Apo-J cells by THP-1 macrophages downregulates TNF-α production. Second, phagocytosis of Apo-J cells by THP-1 macrophages and activation of PI3K/Akt signaling pathway upregulates IL-10 production. Conclusion It is postulated that the phenotypic switch from a proinflammatory M1-like phenotype to an anti-inflammatory M2-like phenotype is dysregulated due to impaired efferocytosis of apoptotic neutrophils at the wound site. Our results demonstrate that NK-4 improves phagocytosis of apoptotic cells, suggesting its potential as a therapeutic strategy to resolve sustained inflammation in chronic wounds.

Download Full-text