Photomodulative effects of low-level laser therapy on tracheal fenestration developed in in vivo model.

The effect of low-level laser therapy (LLLT) on variable mucosal lesions in the upper aerodigestive tract has been reported. However, the effect of LLLT on tracheostomy sites or tracheal fenestration is rarely reported. In this study, we evaluate the effect of LLLT performed using 635 nm laser light based on a cylindrical diffuser and an animal model with tracheal fenestration. An animal model of tracheal fenestration is developed by suturing the trachea to the skin after performing a vertical tracheostomy from the second to the fifth tracheal ring of Wistar rats (male, body weight 200-250 g). LLLT (spot size: 2 cm2) is conducted once daily for five days using a handheld cylindrical device. Twenty-four rats are randomly assigned to a no-therapy or LLLT group with an energy density of 20 J/cm2. Histological analysis is performed at 7 and 14 days after tracheal fenestration. Irradiation at the tracheal fenestration site with an energy density of 20 J/cm2 improves the wound healing, as shown at 2 weeks after tracheostomy. Histological analysis shows significantly decreased acute inflammation and granulation tissue, as well as better cartilage regeneration and less tracheal wall thickening. Therefore, LLLT demonstrates therapeutic potential for preventing tracheal stenosis and granuloma after tracheostomy.

Phlorotannins ameliorate extracellular matrix production in human vocal fold fibroblasts and prevent vocal fold fibrosis via aerosol inhalation in a laser-induced fibrosis model.

Vocal fold fibrosis is an abnormal condition characterized by unfavorable changes in the organization of the extracellular matrix in vocal fold lamina propria. To prevent and treat vocal fold fibrosis, a number of synthetic drugs, such as mitomycin C and the glucocorticoid family, are used after surgery, but these are known to have some side effects. Therefore, using both in vitro and in vivo studies, this study investigated whether phlorotannins extracted from Ecklonia cava have the potential to prevent vocal fold fibrosis with minimal side effects. The results show that phlorotannins suppressed both the expression of the fibrotic phenotypic marker and cell migration by inhibiting the activation of the mitogen-activated protein kinase (MAPK) and Smad2/3 signaling pathways in human vocal fold fibroblasts stimulated by transforming growth factor-ß. Additionally, phlorotannins exhibited antifibrotic efficacy without an excessive inflammatory response in a laser-induced fibrosis rabbit model when delivered as an aerosol via inhalation. Based on these results, phlorotannins should be considered a promising candidate for use in the prevention of vocal fold fibrosis.

Fabrication and biological activity of polycaprolactone/phlorotannin endotracheal tube to prevent tracheal stenosis: An in vitro and in vivo study.

Prolonged endotracheal intubation is the most common cause of tracheal stenosis, which may lead to serious airway obstruction. Development of an endotracheal tube coated with biomaterials that exhibit anti-inflammatory or anti-fibrogenic effects may prevent tracheal stenosis. This study demonstrates that an endotracheal tube coated with phlorotannin, which is present in extracts of the brown alga Ecklonia cava, can prevent tracheal stenosis in a rabbit model. An in vitro study shows that phlorotannin inhibits proliferation of human tracheal fibroblasts treated with transforming growth factor ß1. Phlorotannin-coated endotracheal tubes show steady release of phlorotannin for up to 7 days, and removal of the tube 1 week after insertion reveals a reduction in both fibrogenesis and thickening of tracheal submucosa. Western blot analysis of tracheal tissues after removal of the phlorotannin-coated tube shows decreased protein expression levels of phenotypic markers of fibrosis such as collagen type I and α-smooth muscle actin. The ability of phlorotannin-coated endotracheal tube to prevent tracheal stenosis caused by endotracheal intubation indicates that phlorotannin may be considered as a candidate biomaterial for coating the cuff of endotracheal tubes to prevent tracheal stenosis.

Transoral Low-Level Laser Therapy Via a Cylindrical Device to Treat Oral Ulcers in a Rodent Model.

BACKGROUND AND OBJECTIVE: Various clinical and animal studies have applied low-level laser therapy (LLLT) to treat oral ulcers. However, most previous studies applied lasers with small pinpoint irradiation, which required multiple laser irradiations to cover the complete extent of the ulcer. The objective of this study was to evaluate the effect of LLLT using a 635 nm diode laser via a transoral device to cover the whole lesion on oral ulcers in an animal model. STUDY DESIGN/MATERIALS AND METHODS: An animal model of oral ulcers was developed with a 6 mm skin punch in the right buccal mucosa of Wistar rats (males, body weight 200-250 g). Three days after the mucosal injury, LLLT (spot size 2 cm2 ) was conducted once a day for 5 days. Twenty-eight rats were randomly assigned into four groups according to energy density (control group, 5, 20, 75 J/cm2 ). The size of the ulcers was measured and histologic analysis were performed ten days after the initial mucosal injury. RESULTS: The mean size of the oral ulcers was significantly smaller in rats treated with an energy density of 20 J/cm2 than that of any other group (control group or energy densities of 5 or 75 J/cm2 ). The irradiation of oral ulcers with an energy density of 20 J/cm2 accelerated the oral mucosa wound healing process and decreased inflammation and granulation tissue, resulting in good reepithelization. However, the histologic outcomes of rats irradiated with energy densities of 5 or 75 J/cm2 were comparable with those of the control group. CONCLUSION: LLLT using a 635 nm diode laser for oral ulcers with a transoral cylindrical device for wide light distribution may accelerate the wound healing process. LLLT with large-surface irradiation may be a substitute for previous LLLT for oral mucosal lesions conducted in a punctuate manner. Lasers Surg. Med. © 2019 Wiley Periodicals, Inc.

Development of a reproducible in vivo laser-induced scar model for wound healing study and management.

The aim of the current study was to establish animal scar models in a simple and rapid manner by comparing three methods. Wounds were created on the buttocks of Sprague Dawley rats. For Group 1, the initial wound was created by surgical incision. For Groups 2 and 3, a 1470-nm laser was employed to generate dermal burns as the initial wound. The wounds in Groups 1 and 3 were then sutured for three days. After the wound healing, Group 2 generated the largest collagen proportion with abundant collagen type I and significant increases in α-SMA and TGF-ß1. The proposed method can be an efficient way to develop rat scar models in a simple manner for evaluating scar treatment.

Hypericin-assisted photodynamic therapy against anaplastic thyroid cancer.

BACKGROUND: Hypericin (HYP) extracted from St. John's wort (Hypericum perforatum L.) is a natural photosensitizer in clinical photodynamic therapy (PDT). PDT is one of the powerful methods for cancer treatments because of its excellent tumoritropic characteristics and photosensitizing properties. However, limited reports on the efficacy of PDT on anaplastic thyroid cancer (ATC) have been published. Especially HYP-associated PDT has not been investigated in vitro and in vivo. In this study, we evaluated the effect of HYP for PDT against FRO ATC cells. METHODS: The activities of HYP-assisted PDT were investigated in ATC cells. The ATC FRO cells were treated with a combination of HYP dose and laser power. The viability of FRO cells was measured by MTT assay, and Trypan blue staining was performed to monitor cell death. Detection reactive oxygen species (ROS) and mitochondrial membrane potential after HYP-assisted PDT were analyzed by confocal microscopy. For in vivo study, FRO cells were injected into nude mice. After intravenous injection of HYP, Laser was irradiated and nude mice were monitored in Day 4, 7, 14. RESULTS AND CONCLUSIONS: The rate of FRO cell death was increased by applying HYP dose and laser power dependent. Moreover, HYP and laser irradiation induced FRO cell death was mediated by the intracellular ROS generation and mitochondrial damage. Finally, the HYP-assisted PDT eliminated FRO cell tumor from the mouse in vivo. These data demonstrate that HYP could be an effective photosensitizer for human ATC therapy.