scholarly journals Argon- and nitrogen-plasma pulses decrease facial sebum excretion in oily human skin by regulating lipogenesis and proliferation in human sebocytes

Author(s):  
Sung Bin Cho ◽  
Seung-Ju Lee ◽  
Dae San Yoo ◽  
Song-Ee Kim ◽  
Christos C. Zouboulis ◽  
...  

Abstract Although several energy devices targeting sebaceous glands have been developed, an effective and safe therapeutic tool for hyperseborrhea is needed. Non-thermal atmospheric-pressure plasma (NTAPP) induces microscopic tissue reactions in sebaceous glands of rat skin in vivo. Fifteen healthy volunteers with oily facial skin underwent three sessions of argon- and nitrogen-NTAPP treatment. The casual sebum level, sebum excretion rate, porphyrin index, and histological analysis were evaluated. Argon- and nitrogen-NTAPP pulses were applied to testosterone and linoleic acid (T/LA)-treated human SZ95 sebocytes. Lipids were assessed using BODIPY and quantitative Nile red staining. Proliferation and differentiation markers were assessed. Argon- and nitrogen-NTAPP pulses suppressed casual sebum levels and sebum excretion rates in the skin, at week 4. The porphyrin index revealed a 38% reduction at week 2. Skin biopsy samples showed no obvious thermal coagulation, but the number of Ki67+ cells in the sebaceous glands decreased at week 2. Argon- and nitrogen-NTAPP inhibited T/LA-induced increases in lipid synthesis, Ki67+ cells, and peroxisome proliferator-activated receptor-ɣ transcription in human sebocytes without apoptosis. Argon- and nitrogen-NTAPP therapy is a safe and effective method for reducing sebum excretion in oily human skin and inhibits lipogenesis and cell proliferation in human sebocytes.

Dermatology ◽  
2020 ◽  
pp. 1-5
Author(s):  
Christos C. Zouboulis ◽  
Síona Ní Raghallaigh ◽  
Gerd Schmitz ◽  
Frank C. Powell

Background: Despite their widespread clinical use in both acne vulgaris and rosacea, the effects of tetracyclines on sebocytes have not been investigated until now. Sebaceous glands are central to the pathogenesis of acne and may be important in the development of rosacea. Objective: The aim of this study was to assess the effects of doxycycline on the immortalized SZ95 sebaceous gland cell line as a model for understanding possible effectiveness on the sebaceous glands in vivo. Methods: The effects of doxycycline on SZ95 sebocyte numbers, viability, and lipid content as well as its effects on the mRNA levels of peroxisome proliferator-activated receptors α and γ, in comparison to the peroxisome proliferator-activated receptor γ agonist troglitazone, were investigated. Results: Doxycycline reduced the cell number and increased the lipid content of SZ95 sebocytes in vitro after 2 days of treatment. These doxycycline effects may be explained by an upregulation of peroxisome proliferator-activated receptor γ mRNA levels at 12 and 24 h, whereas troglitazone already upregulated peroxisome proliferator-activated receptor γ levels after 6 h. Both compounds did not influence peroxisome proliferator-activated receptor α mRNA levels. Conclusion: These new findings illustrate a previously unknown effect of doxycycline on sebocytes, which may be relevant to their modulation of disorders of the pilosebaceous unit, such as acne vulgaris and rosacea.


2009 ◽  
Vol 296 (5) ◽  
pp. F1146-F1157 ◽  
Author(s):  
S. S. Ghosh ◽  
H. D. Massey ◽  
R. Krieg ◽  
Z. A. Fazelbhoy ◽  
S. Ghosh ◽  
...  

TNF-α and NF-κB play important roles in the development of inflammation in chronic renal failure (CRF). In hepatic cells, curcumin is shown to antagonize TNF-α-elicited NF-κB activation. In this study, we hypothesized that if inflammation plays a key role in renal failure then curcumin should be effective in improving CRF. The effectiveness of curcumin was compared with enalapril, a compound known to ameliorate human and experimental CRF. Investigation was conducted in Sprague-Dawley rats where CRF was induced by 5/6 nephrectomy (Nx). The Nx animals were divided into untreated (Nx), curcumin-treated (curcumin), and enalapril-treated (enalapril) groups. Sham-operated animals served as a control. Renal dysfunction in the Nx group, as evidenced by elevated blood urea nitrogen, plasma creatinine, proteinuria, segmental sclerosis, and tubular dilatation, was significantly reduced by curcumin and enalapril treatment. However, only enalapril significantly improved blood pressure. Compared with the control, the Nx animals had significantly higher plasma and kidney TNF-α, which was associated with NF-κB activation and macrophage infiltration in the kidney. These changes were effectively antagonized by curcumin and enalapril treatment. The decline in the anti-inflammatory peroxisome proliferator-activated receptor γ (PPARγ) seen in Nx animals was also counteracted by curcumin and enalapril. Studies in mesangial cells were carried out to further establish that the anti-inflammatory effect of curcumin in vivo was mediated essentially by antagonizing TNF-α. Curcumin dose dependently antagonized the TNF-α-mediated decrease in PPARγ and blocked transactivation of NF-κB and repression of PPARγ, indicating that the anti-inflamatory property of curcumin may be responsible for alleviating CRF in Nx animals.


2018 ◽  
Vol 15 (4) ◽  
pp. 345-354 ◽  
Author(s):  
Barbara D'Orio ◽  
Anna Fracassi ◽  
Maria Paola Cerù ◽  
Sandra Moreno

Background: The molecular mechanisms underlying Alzheimer's disease (AD) are yet to be fully elucidated. The so-called “amyloid cascade hypothesis” has long been the prevailing paradigm for causation of disease, and is today being revisited in relation to other pathogenic pathways, such as oxidative stress, neuroinflammation and energy dysmetabolism. The peroxisome proliferator-activated receptors (PPARs) are expressed in the central nervous system (CNS) and regulate many physiological processes, such as energy metabolism, neurotransmission, redox homeostasis, autophagy and cell cycle. Among the three isotypes (α, β/δ, γ), PPARγ role is the most extensively studied, while information on α and β/δ are still scanty. However, recent in vitro and in vivo evidence point to PPARα as a promising therapeutic target in AD. Conclusion: This review provides an update on this topic, focussing on the effects of natural or synthetic agonists in modulating pathogenetic mechanisms at AD onset and during its progression. Ligandactivated PPARα inihibits amyloidogenic pathway, Tau hyperphosphorylation and neuroinflammation. Concomitantly, the receptor elicits an enzymatic antioxidant response to oxidative stress, ameliorates glucose and lipid dysmetabolism, and stimulates autophagy.


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