<i>Cryptotanshinone</i> reduces psoriatic epidermal hyperplasia via inhibiting the activation of <scp>STAT</scp>3

Tang, Lin; He, Shuping; Wang, Xieqi; Liu, Hongying; Zhu, Ying; Feng, Bing; Su, Zuowei; Zhu, Wei; Liu, Bo; Xu, Fangfang; Li, Chutian; Zhao, Jie; Zheng, Xiaobin; Lu, Chuanjian; Zheng, Guangjuan

doi:10.1111/exd.13511

Cited by 32 publications

(18 citation statements)

References 41 publications

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“…Keratin 17 is up‐regulated in psoriatic skin, and antagonists of IL‐17A and IL‐17RA decreased keratin 17 expression levels . In lines with these findings, inhibition of STAT3 activation reduced keratin 17 expression and psoriasiform lesions in mice . Our study showed that 5(OH)Trp markedly inhibited p‐Erk1/2 and p‐STAT3 expression in HaCaT cells and primary keratinocytes, and significantly improved the psoriasiform lesions.…”

Section: Discussionsupporting

confidence: 86%

5‐hydroxytryptophan attenuates imiquimod‐induced psoriasiform dermatitis probably through inhibition of IL‐17A production and keratinocyte activation

Hsu

Yang

et al. 2018

Experimental Dermatology

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Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that 5-hydroxytryptophan (5(OH)Trp), a tryptophan metabolite, alleviated collagen-induced arthritis and suppressed cytokine production. In this study, we evaluated the effects of 5(OH)Trp in a mouse model for psoriasiform dermatitis, induced by imiquimod (IMQ). We showed that 5(OH)Trp significantly reduced the cumulative scores, epidermal thickness and ki-67 expression in the skin. In addition, 5(OH)Trp decreased local and systemic inflammation. Moreover, 5(OH)Trp significantly inhibited keratinocyte activation with decrease in IL-6 production and p-Erk1/2 and p-STAT3 expression. 5(OH)Trp also inhibited the differentiation of IFN-γ- and IL-17A-expressing CD4 T cells and related cytokine production (TNF-α, IL-6, IL-17A and IFN-γ) in splenocytes. In conclusion, 5(OH)Trp can inhibit imiquimod-induced psoriasiform dermatitis in mice and inhibit activation in keratinocytes and splenocytes.

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Section: Discussionsupporting

confidence: 86%

5‐hydroxytryptophan attenuates imiquimod‐induced psoriasiform dermatitis probably through inhibition of IL‐17A production and keratinocyte activation

Hsu

Yang

et al. 2018

Experimental Dermatology

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“…Cryptotanshinone (CT) is isolated from the plant Salvia miltiorrhiza Bunge and has been identified to block STAT3 phosphorylation and homodimerization . CT has been demonstrated to have anti‐tumor activities in various malignancies, including breast cancer,liver cancer,prostate cancer, and ovarian cancer .…”

Section: Introductionmentioning

confidence: 99%

“…Cryptotanshinone (CT) is isolated from the plant Salvia miltiorrhiza Bunge and has been identified to block STAT3 phosphorylation and homodimerization. [7][8][9] CT has been demonstrated to have anti-tumor activities in various malignancies, including breast cancer,liver cancer,prostate cancer, and ovarian cancer. [10][11][12][13] CT was found to induced apoptosis and cell cycle arrest in gastric cancer cells via reactive oxygen species (ROS)-mediated MAPK and AKT signaling pathways.…”

mentioning

confidence: 99%

Cryptotanshinone suppresses cell proliferation and glucose metabolism via STAT3/SIRT3 signaling pathway in ovarian cancer cells

et al. 2018

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Ovarian cancer is the most malignant gynecologic cancer among women worldwide. Cryptotanshinone (CT), isolated from Salvia miltiorrhiza Bunge, has been identified as a potential therapeutic agent in treating several malignant tumors, but the molecular mechanism of CT in ovarian cancer still remains illustrated. Here, we sought to elucidate the regulatory function of CT on cell glucose metabolism in ovarian cancer. The treatment of CT on ovarian cancer cells effectively inhibited glucose uptake and lactate production in ovarian cancer cells. The expression levels of glycolysis‐related proteins, such as GLUT1, LDHA, and HK2, were decreased by the treatment of CT detected by qRT‐PCR and immunoblotting. Mechanistically, CT exerted its anti‐tumor effect by targeting STAT3/SIRT3/HIF‐1α signaling pathway in vitro and in vivo, which could be rescued by the introduction of SIRT3 shRNA in ovarian cancer cells. The clinical data showed that the expression level of STAT3 in ovarian cancer patients’ sera and tissues was positively correlated with those of GLUT1, LDHA, HK2 and HIF‐1α, but negatively with that of SIRT3These findings provide evidence that CT inhibited cellular glycolysis‐induced cell growth and proliferation through repression of STAT3/SIRT3/HIF‐1α signaling pathway, indicating that CT may be developed as a chemotherapeutic agent to treat ovarian cancer.

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“…Transgenic mice constitutively over-expressing STAT3 in keratinocytes develop cutaneous lesions reminiscent of human psoriatic lesions [ 30 , 31 ]. Thus, STAT3 is a well-established potential drug target to treat psoriasis [ 31 , 33 , 34 ]. In M1 and M2 macrophages OA-NO 2 inhibits the activation of STAT1, STAT3, and STAT6 when activated by LPS and IL-4 [ 35 ].…”

Section: Resultsmentioning

confidence: 99%

Electrophilic nitro-fatty acids suppress psoriasiform dermatitis: STAT3 inhibition as a contributory mechanism

et al. 2021

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Psoriasis is a chronic inflammatory skin disease with no cure. Although the origin of psoriasis and its underlying pathophysiology remain incompletely understood, inflammation is a central mediator of disease progression. In this regard, electrophilic nitro-fatty acids (NO 2 –FAs) exert potent anti-inflammatory effects in several in vivo murine models of inflammatory diseases, such as chronic kidney disease and cardiovascular disease. To examine the therapeutic potential of NO 2 –FAs on psoriasiform dermatitis, we employed multiple murine models of psoriasis. Our studies demonstrate that oral treatment with nitro oleic acid (OA-NO 2 ) has both preventative and therapeutic effects on psoriasiform inflammation. In line with this finding, oral OA-NO 2 downregulated the production of inflammatory cytokines in the skin. In vitro experiments demonstrate that OA-NO 2 decreased both basal IL-6 levels and IL-17A-induced expression of IL-6 in human dermal fibroblasts through the inhibition of NF-κB phosphorylation. Importantly, OA-NO 2 diminished STAT3 phosphorylation and nuclear translocation via nitroalkylation of STAT3, which inhibited keratinocyte proliferation. Overall, our results affirm the critical role of both NF-κB and STAT3 in the incitement of psoriasiform dermatitis and highlight the pharmacologic potential of small molecule nitroalkenes for the treatment of cutaneous inflammatory diseases, such as psoriasis.

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Cryptotanshinone reduces psoriatic epidermal hyperplasia via inhibiting the activation of STAT3

Cited by 32 publications

References 41 publications

5‐hydroxytryptophan attenuates imiquimod‐induced psoriasiform dermatitis probably through inhibition of IL‐17A production and keratinocyte activation

5‐hydroxytryptophan attenuates imiquimod‐induced psoriasiform dermatitis probably through inhibition of IL‐17A production and keratinocyte activation

Cryptotanshinone suppresses cell proliferation and glucose metabolism via STAT3/SIRT3 signaling pathway in ovarian cancer cells

Electrophilic nitro-fatty acids suppress psoriasiform dermatitis: STAT3 inhibition as a contributory mechanism

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