Mechanisms of Acantholysis in Pemphigus: Mechanical or Inflammatory?

Pemphigus is a rare autoimmune disease, involving the skin and mucous epithelia, characterized by flaccid blisters and erosions. Histologically, the basic abnormality in all forms of pemphigus is the separation of keratinocytes from one another, a process known as acantholysis. There is direct evidence that autoantibodies against desmoglein, a transmembrane desmosomal component, are critical in its pathogenesis, but the exact mechanism that induces acantholysis is yet unknown. Actually, different studies suggest three possible mechanisms: sterical impedance, intracellular signalling and apoptosis. Understanding these processes should show new therapeutic perspective

Protective Effects of Pinus halepensis Bark Extract and Nicotine on Cigarette Smoke-induced Oxidative Stress in Keratinocytes

Background/Aim: Cigarette smoke (CS) is a major environmental health threat. The oxidative stress induced by CS on keratinocytes and the possible protective effect of nicotine, its receptor inhibitors, and Pinus halepensis bark extract in relation to known antioxidants were investigated. Materials and Methods: Primary mouse keratinocytes were exposed to cigarette smoke in the presence and absence of Pinus halepensis bark extract (1 μg/ml), rutin (50 μΜ) and ascorbic acid (250 μΜ), nicotine (1 μM) with or without mecamylamine (5 μM) and α-bungarotoxin (0.1 μΜ). Keratinocyte viability and oxidative stress were evaluated by MTT and fluorescence assays. Results: Pinus halepensis bark extract decreased the oxidative stress and increased the viability of keratinocytes, and moreover, these effects were more pronounced compared to the mixture of rutin and Lascorbic acid. Nicotine significantly enhanced the viability potentiation of the beneficial effect induced by Pinus halepensis bark extract. Mecamylamine and α-bungarotoxin showed no specific effect. Conclusion: Pinus halepensis bark extract in combination with nicotine may successfully reverse skin damage induced by cigarette smoke. © 2020 International Institute of Anticancer Research. All rights reserved