Terminalia Chebulanin Attenuates Psoriatic Skin Lesion via Regulation of Heme Oxygenase-1

An, Jingang; Li, Tian; Dong, Yingying; Li, Zhengxiao

doi:10.1159/000445645

Cited by 27 publications

(16 citation statements)

References 37 publications

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“…IL-17A is a critical cytokine involved in the pathogenesis of AD. 29,30 Its expression in keratinocytes was reported [31][32][33] and detected in our primary culture (see Fig E4, B). CXCL10 mediates cell adhesion, migration, and inflammatory infiltrates in patients with AD.…”

Section: Expression Of Bnp and Its Receptors Is Increased In The Skinsupporting

confidence: 66%

New mechanism underlying IL-31–induced atopic dermatitis

Meng

Moriyama

Feld

et al. 2018

Journal of Allergy and Clinical Immunology

145

151

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Section: Expression Of Bnp and Its Receptors Is Increased In The Skinsupporting

confidence: 66%

New mechanism underlying IL-31–induced atopic dermatitis

Meng

Moriyama

Feld

et al. 2018

Journal of Allergy and Clinical Immunology

145

151

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“…IL-17 plays important roles in the pathogenesis of psoriasis and IL-17 inhibitors are considered important agents in the management of psoriasis [35][36][37][38]. The RT-PCR results in our study showed that IMQ induced the up-regulation of IL-17 A mRNA and IL-17 F mRNA in mouse skin, whereas ZnPc-F7-PDT down-regulated their expression, which is another potential mechanism of ZnPc-F7-PDT in the treatment of psoriasis.…”

Section: Discussionmentioning

confidence: 99%

Anti-Psoriasis Effects and Mechanisms of Α-(8-Quinolinoxy) Zinc Phthalocyanine-Mediated Photodynamic Therapy

Liu

Wang²,

et al. 2017

Cell Physiol Biochem

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Background/Aims: The aim of this study was to determine the anti-psoriasis effects of α-(8-quinolinoxy) zinc phthalocyanine (ZnPc-F7)-mediated photodynamic therapy (PDT) and to reveal its mechanisms. Methods: HaCaT cells were used to observe the influence of ZnPc-F7-PDT on cell proliferation in vitro. The in vivo anti-psoriasis effects of ZnPc-F7-PDT were evaluated using a mouse vagina model, a propranolol-induced cavy psoriasis model and an imiquimod (IMQ)-induced nude mouse psoriasis model. Flow cytometry was carried out to determine T lymphocyte levels. Western blotting was performed to determine protein expression, and a reverse transcription-polymerase chain reaction test was performed to determine mRNA expression. Results: The results showed that ZnPc-F7-PDT significantly inhibited the proliferation of HaCaT cells in vitro; when the light doses were fixed, changing the irradiation time or output power had little influence on the inhibition rate. ZnPc-F7-PDT significantly inhibited the hyperproliferation of mouse vaginal epithelium induced by diethylstilbestrol and improved propranolol-and IMQ-induced psoriasis-like symptoms. ZnPc-F7-PDT inhibited IMQ-induced splenomegaly and T lymphocyte abnormalities. ZnPc-F7-PDT did not appear to change T lymphocytes in the mouse vagina model. ZnPc-F7-PDT downregulated the expression of proliferating cell nuclear antigen (PCNA), B-cell lymphoma-2 (Bcl-2), interleukin (IL)-17A mRNA and IL-17F mRNA, and up-regulated the expression of Bax. Conclusion: In conclusion, ZnPc-F7-PDT exhibited therapeutic effects in psoriasis both in vitro and in vivo and is a potential approach in the treatment of psoriasis. Potential mechanisms of these effects included the inhibition of hyperproliferation; regulation of PCNA, Bcl-2, Bax, IL-17A mRNA and IL-17F mRNA expression; and immune regulation.

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“…Hence, lack of good knowledge of etiopathogenesis impairs the development of an effective treatment. However, recent studies of molecular mechanisms in psoriatic patients give a new promise for effective therapy [25][26][27].…”

Section: Introductionmentioning

confidence: 99%

Psoriasis Treatment Changes the Expression Profile of Selected Caspases and their Regulatory MicroRNAs

Wcisło‐Dziadecka¹,

Simka²,

Kaźmierczak³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Psoriasis, an autoimmune diseases of the skin, characterized by patches of abnormal/inflammed skin, although not usually life-threatening, it causes severe discomfort, esthetic impairments, and may lead to impaired social functions and social withdrawal. Besides UV-phototherapy, various anti-inflammatory treatments are applied, depending on the severity of symptoms. In 2008, adalimumab (fully humanized human anti-TNF antibody) was launched for the treatment of psoriasis. In the quest to better understand the pathomechanism of adalimumab’s therapeutic effects, and the acquired resistance to the drug, we have investigated how its administration affect the regulation of the expression of selected caspases, including those activated by inflammosome. Methods: The research was initially carried out on normal human dermal fibroblasts (NHDF) treated with adalimumab for 2, 8 and 24 hours in vitro. Then, expression profile of genes encoding caspases and their regulatory micro-RNAs was determined with the use of oligonucleotide microarray. The validation of the microarray results was carried out by qRT-PCR. The in vitro study was followed by ex-vivo investigation of adalimumab’s effects on the expression of caspase-6 in blood of the psoriatic patients. The samples were collected before, and 2 hours after adalimumab’s administration and the analysis was determined by qRT-PCR. Results: The result of the analysis indicated that introduction of adalimumab to the NHDF culture resulted in the change of the transcription activity of genes encoding caspases and genes encoding miRNAs. The analysis revealed 5 different miRNA molecules regulating the expression of: CASP2, CASP3 and CASP6. There were no statistically significant differences in the expression of gene encoding caspase-6 in the patients’ blood before and 2 hours after the anti-TNF drug administration. Conclusion: We have found that adalimumab administration affects caspases expression, thus they may be used as molecular markers for monitoring the therapy with the use of an anti-TNF drugs, including adalimumab. It is likely that the mechanisms responsible for changed expression profiles of genes encoding caspase-2,-3, and -6, may be caused by the upregulation of the respective microRNA molecules. Increased expression of genes encoding specific caspases may induce inflammatory processes, as well as trigger apoptosis. Furthermore, the proapoptotic activity of caspases may be enhanced by miRNA molecules, which exhibit proapoptotic function. The overexpression of such miRNAs was observed in our study.

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Terminalia Chebulanin Attenuates Psoriatic Skin Lesion via Regulation of Heme Oxygenase-1

Cited by 27 publications

References 37 publications

New mechanism underlying IL-31–induced atopic dermatitis

New mechanism underlying IL-31–induced atopic dermatitis

Anti-Psoriasis Effects and Mechanisms of Α-(8-Quinolinoxy) Zinc Phthalocyanine-Mediated Photodynamic Therapy

Psoriasis Treatment Changes the Expression Profile of Selected Caspases and their Regulatory MicroRNAs

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