ABSTRACT
The ancient Chinese medical book "Compendium of Materia Medica" records that pears can relieve symptoms of respiratory-related diseases. Previous research has shown that pear Pyrus Pyrifolia (Burm.f.) Nakai has antioxidant and anti-inflammatory properties. However, the anti-inflammatory, antioxidant, and anti-photoaging protective effects of Pyrus pyrifolia (Burm.f.) Nakai seed components have not been studied. Ultraviolet light (UV) causes skin inflammation, damages the skin barrier, and is an important cause of skin photoaging. Therefore, UV light with a wavelength of 365 nm was used to irradiate HaCaT and mice. Western blot, real-time quantitative polymerase chain reaction, and fluorescence imaging system were used to explore its anti-UVA mechanism. Dialysis membrane and nuclear magnetic resonance were used for the chemical constituent analysis of pear seed water extract (PSWE). We found that PSWE can significantly reduce UVA-induced skin cell death and mitogen-activated protein kinase phosphorylation and can inhibit the mRNA expression of UVA-induced cytokines (including IL-1ß, IL-6, and TNF-α). In addition, PSWE can also reduce the generation of oxidative stress within skin cells. In vivo experimental studies found that PSWE pretreatment effectively reduced transepidermal water loss, inflammation, redness, and dryness in hairless mice. The molecular weight of the active part of pear water extract is approximately 384. Based on the above results, we first found that pear seeds can effectively inhibit oxidative stress and damage caused by UVA. It is a natural extract with antioxidant properties and anti-aging activity that protects skin cells and strengthens the skin barrier.
ABSTRACT
Split-thickness skin grafting (STSG) is a frontline treatment for challenging surgical wounds, including diabetic foot ulcers, venous leg ulcers, and post-surgical defects. This study explores the use of STSG employing the pinch graft technique for hard-to-heal surgical wounds following Mohs micrographic surgery (MMS). An 83-year-old patient with a non-improving post-MMS defect on the left lower leg underwent STSG from the right inner thigh using the pinch graft technique. The grafts were secured with a mesh dressing, adhesive strips, and compression bandaging. The patient experienced complete re-epithelialization and reduced pain within five weeks, emphasizing the efficacy of STSG for challenging cases. This case underscores the importance of considering STSG, especially in challenging locations, as a rapid and efficient treatment with improved quality of life. The pinch graft technique is presented as a useful option following MMS. This study encourages Mohs surgeons to consider STSG for reconstruction in challenging locations, especially on the lower leg.
ABSTRACT
Boswellic acids, triterpenoids derived from the genus Boswellia (Burseraceae), are known for their anti-inflammatory and anti-tumor efficacy. Atopic dermatitis is a chronic, non-infectious inflammatory skin disease. However, the effects of α-boswellic acid on atopic dermatitis have not been studied. Therefore, in this study we examined the expression level of pro-inflammatory cytokines, histopathological analysis, and physiological data from BALB/c mice with atopic-like dermatitis induced by 2,4-dinitrochlorobenzene and TNF-α/IFN-γ-stimulated HaCaT cells to better understand the agent's anti-atopic dermatitis efficacy. First, we found that α-boswellic reduced the epidermal thickening, mast cell numbers, and dermal infiltration of 2,4-dinitrochlorobenzene-induced atopic-like dermatitis in BALB/c mice. Furthermore, we also found that α-boswellic acid can restore transepidermal water loss and skin reddening in mice. In human keratinocytes inflamed by TNF-α/IFN-γ, α-boswellic acid inhibited MAP kinase activation and showed a reduction in NF-κB nuclear translocation. Finally, α-boswellic acid can reduce the expression level of cytokines (IL-1ß, IL-6, and IL-8) following the stimulation of TNF-α/IFN-γ in HaCaT cells. Taken together, our study suggests that α-boswellic acids are a potential component for the development of anti-atopic dermatitis drugs.
Subject(s)
Dermatitis, Atopic , Triterpenes , Animals , Cytokines/metabolism , Dermatitis, Atopic/chemically induced , Dermatitis, Atopic/drug therapy , Dermatitis, Atopic/metabolism , Dinitrochlorobenzene/toxicity , HaCaT Cells , Humans , Interferon-gamma/genetics , Interferon-gamma/metabolism , Mice , Mice, Inbred BALB C , NF-kappa B/metabolism , Plant Extracts/pharmacology , Skin/metabolism , Triterpenes/metabolism , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Ultraviolet rays are the main cause of skin aging. Isoflavone structures are good anti-ultraviolet natural compounds and have an especially strong anti-ultraviolet B (UVB) effect. However, the anti-ultraviolet A (UVA) effect of isoflavones is more controversial. Therefore, this study aims to discover which isoflavone analogue possesses a strong anti-ultraviolet A. We found the isoflavonoid intermediate deoxybenzoin-3A (DOB-3A) to be a similar isoflavone structural compound with strong anti-ultraviolet A effects. Ultraviolet rays with a wavelength of 350 nm are used to irradiate the fibroblasts of the human skin. Western blot, flow cytometry, and transmission electron microscope analyses were used to explore its anti-ultraviolet A mechanism. We established the results that DOB-3A (1) reduced the death of fibroblasts caused by ultraviolet A, (2) avoided the damage to the organelles and structures after UVA irradiation, (3) inhibited the generation of intracellular reactive oxygen species (ROS) and hydrogen peroxide-induced damage, and (4) decreased the phosphorylation of mitogen-activated protein kinases (MAPK) caused by UVA. Based on the above findings, DOB-3A is a very good anti-ultraviolet A isoflavone-related structure. Because it is simple to synthesize and has good effects, DOB-3A is a suitable anti-ultraviolet A product with an isoflavone structure. Moreover, DOB-3A's structure provides a reference for the synthesis of anti-UVA isoflavones.
Subject(s)
Dermis/drug effects , Fibroblasts/drug effects , Ultraviolet Rays , Dermis/metabolism , Fibroblasts/metabolism , Humans , Hydrogen Peroxide/antagonists & inhibitors , Hydrogen Peroxide/pharmacology , Mitogen-Activated Protein Kinases/antagonists & inhibitors , Mitogen-Activated Protein Kinases/metabolism , Molecular Structure , Phosphorylation/drug effects , Reactive Oxygen Species/antagonists & inhibitors , Reactive Oxygen Species/metabolismABSTRACT
BACKGROUND: Cutaneous angiosarcoma (CAS) is a rare, malignant tumor of vascular mesenchymal origin accounting for less than 1% of all sarcomas. OBJECTIVE: To examine epidemiologic trends and outcomes in CAS. METHODS: In this retrospective, population-based study, patients with CAS were identified from the Surveillance Epidemiology and End Results database. Age, sex, and race-standardized incidence rates (IRs) were calculated. Survival was assessed with Kaplan-Meier curves and Cox proportional hazards models. RESULTS: Of 811 patients with CAS, 43% had a prior primary cancer. CAS IR for patients without prior primary cancers dropped from 5.88 per 100,000 in 1973 to 1984 to 2.87 per 100,000 in 2005 to 2014. In those with prior primary cancers, IR rose from 0.03 per 100,000 in 1973 to 1984 to 2.25 per 100,000 in 2005 to 2014. On multivariate analysis, patients older than 70 years of age had a higher risk of death compared with those younger than 50 years (hazard ratio, 2.16; 95% confidence interval 1.33-3.57; P = .002), and distant disease was associated with increased risk of death compared with localized disease (hazard ratio, 1.50; 95% confidence interval, 1.11-2.03; P = .008). Receipt of surgery and/or radiation therapy was not associated with survival. LIMITATIONS: Potential selection and miscoding bias, retrospective nature. CONCLUSION: CAS rates are rising among those with other prior primary cancers. Survival is not affected by current therapeutic strategies, highlighting the need for additional treatment options.
Subject(s)
Hemangiosarcoma/epidemiology , Neoplasms, Second Primary/epidemiology , Skin Neoplasms/epidemiology , Age Factors , Aged , Aged, 80 and over , Chemoradiotherapy, Adjuvant/statistics & numerical data , Chemotherapy, Adjuvant/methods , Chemotherapy, Adjuvant/statistics & numerical data , Dermatologic Surgical Procedures/statistics & numerical data , Female , Hemangiosarcoma/therapy , Humans , Incidence , Kaplan-Meier Estimate , Male , Middle Aged , Neoadjuvant Therapy/methods , Neoadjuvant Therapy/statistics & numerical data , Neoplasms, Second Primary/therapy , Prognosis , Retrospective Studies , Risk Factors , SEER Program/statistics & numerical data , Skin Neoplasms/therapy , Survival Rate , United States/epidemiologyABSTRACT
There are many hair disorders, all of which involve alterations in normal hair biology. Essentially, hair disorders involve changes to hair fiber caliber, density per unit area, and/or the duration of anagen and telogen in the hair growth cycle. Hair disorders may be triggered by inflammation, genetics, the environment, or hormones; the relative contributions of these factors vary for different hair disorder diagnoses. Suitable treatments may either address the underlying causal factors or directly act on hair follicle biology. The objectives are to normalize the hair growth cycle, modulate the size of hair follicles, and potentially regenerate hair follicles to stabilize hair density. The purpose of this manuscript is to review the basic biology of the hair follicle, as well as causal mechanisms for the disordered hair follicle using some selected examples of hair disorders.