Fingolimod hydrochloride gel shows promising therapeutic effects in a mouse model of atopic dermatitis

2016 ◽  
Vol 68 (10) ◽  
pp. 1268-1277
Author(s):  
Mayurkumar Tamakuwala ◽  
Warren Ratna ◽  
Amit Joshi ◽  
Grazia Stagni
Keyword(s):  
Atopic Dermatitis ◽  
Mouse Model ◽  
Therapeutic Effects ◽  
Fingolimod Hydrochloride

scholarly journals Therapeutic effects of quinine in a mouse model of atopic dermatitis

2021 ◽  
Vol 23 (5) ◽  
Author(s):  
Qian Zhang ◽  
Hongjing Jiang ◽  
Miao Liu ◽  
Xinchen Li ◽  
Murong Zhou ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Mouse Model ◽  
Therapeutic Effects

scholarly journals Therapeutic Effects of Tonsil-derived Mesenchymal Stem Cells in an Atopic Dermatitis Mouse Model

In Vivo ◽  
2021 ◽  
Vol 35 (2) ◽  
pp. 845-857
Author(s):  
HARRY JUNG ◽  
GIL MYEONG SON ◽  
JAE JUN LEE ◽  
HAE SANG PARK
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Atopic Dermatitis ◽  
Mouse Model ◽  
Therapeutic Effects

Treatment of atopic dermatitis with Chinese herbal medicine. Therapeutic effects of Hochuekkitou.

1989 ◽  
Vol 51 (5) ◽  
pp. 1003-1013 ◽  
Author(s):  
Hiromi KOBAYASHI ◽  
Masamitsu ISHII ◽  
Tsukasa TANII ◽  
Takeshi KOHNO ◽  
Toshio HAMADA
Keyword(s):  
Atopic Dermatitis ◽  
Herbal Medicine ◽  
Chinese Herbal Medicine ◽  
Therapeutic Effects ◽  
Chinese Herbal

Therapeutic Effects of Olopatadine Hydrochloride on Blood Substance P Levels and Circulating Th17 Cell Numbers in Patients with Atopic Dermatitis

2010 ◽  
Vol 72 (2) ◽  
pp. 159-162
Author(s):  
Rieko KABASHIMA ◽  
Toshinori BITO ◽  
Makiko TAJIRI ◽  
Chika KAWAKAMI ◽  
Shoko FUKAMACHI ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Substance P ◽  
Th17 Cell ◽  
Therapeutic Effects ◽  
Cell Numbers ◽  
Olopatadine Hydrochloride

scholarly journals Neuroimaging, Urinary, and Plasma Biomarkers of Treatment Response in Huntington’s Disease: Preclinical Evidence with the p75NTR Ligand LM11A-31

2021 ◽  
Author(s):  
Danielle A. Simmons ◽  
Brian D. Mills ◽  
Robert R. Butler III ◽  
Jason Kuan ◽  
Tyne L. M. McHugh ◽  
...  
Keyword(s):  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Treatment Response ◽  
Diffusion Tensor ◽  
Disease Onset ◽  
Therapeutic Effects ◽  
Plasma Cytokine ◽  
Cytokine Levels ◽  
Pharmacodynamic Biomarkers

AbstractHuntington’s disease (HD) is caused by an expansion of the CAG repeat in the huntingtin gene leading to preferential neurodegeneration of the striatum. Disease-modifying treatments are not yet available to HD patients and their development would be facilitated by translatable pharmacodynamic biomarkers. Multi-modal magnetic resonance imaging (MRI) and plasma cytokines have been suggested as disease onset/progression biomarkers, but their ability to detect treatment efficacy is understudied. This study used the R6/2 mouse model of HD to assess if structural neuroimaging and biofluid assays can detect treatment response using as a prototype the small molecule p75NTR ligand LM11A-31, shown previously to reduce HD phenotypes in these mice. LM11A-31 alleviated volume reductions in multiple brain regions, including striatum, of vehicle-treated R6/2 mice relative to wild-types (WTs), as assessed with in vivo MRI. LM11A-31 also normalized changes in diffusion tensor imaging (DTI) metrics and diminished increases in certain plasma cytokine levels, including tumor necrosis factor-alpha and interleukin-6, in R6/2 mice. Finally, R6/2-vehicle mice had increased urinary levels of the p75NTR extracellular domain (ecd), a cleavage product released with pro-apoptotic ligand binding that detects the progression of other neurodegenerative diseases; LM11A-31 reduced this increase. These results are the first to show that urinary p75NTR-ecd levels are elevated in an HD mouse model and can be used to detect therapeutic effects. These data also indicate that multi-modal MRI and plasma cytokine levels may be effective pharmacodynamic biomarkers and that using combinations of these markers would be a viable and powerful option for clinical trials.

MR1‐dependent immune surveillance of the skin contributes to pathogenesis and is a photobiological target of UV light therapy in a mouse model of atopic dermatitis.

Allergy ◽  
2021 ◽  
Author(s):  
Karmella Naidoo ◽  
Katherine Woods ◽  
Christophe Pellefigues ◽  
Alissa Cait ◽  
David O’Sullivan ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Mouse Model ◽  
Uv Light ◽  
Immune Surveillance ◽  
Light Therapy

scholarly journals A novel phosphoramide compound, DCZ0805, shows potent anti-myeloma activity via the NF-κB pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xuejie Gao ◽  
Bo Li ◽  
Anqi Ye ◽  
Houcai Wang ◽  
Yongsheng Xie ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tumor Burden ◽  
High Rate ◽  
Cell Counting ◽  
Tumor Xenograft ◽  
Luciferase Reporter ◽  
Therapeutic Effects ◽  
Xenograft Mouse Model

Abstract Background Multiple myeloma (MM) is a highly aggressive and incurable clonal plasma cell disease with a high rate of recurrence. Thus, the development of new therapies is urgently needed. DCZ0805, a novel compound synthesized from osalmide and pterostilbene, has few observed side effects. In the current study, we intend to investigate the therapeutic effects of DCZ0805 in MM cells and elucidate the molecular mechanism underlying its anti-myeloma activity. Methods We used the Cell Counting Kit-8 assay, immunofluorescence staining, cell cycle assessment, apoptosis assay, western blot analysis, dual-luciferase reporter assay and a tumor xenograft mouse model to investigate the effect of DCZ0805 treatment both in vivo and in vitro. Results The results showed that DCZ0805 treatment arrested the cell at the G0/G1 phase and suppressed MM cells survival by inducing apoptosis via extrinsic and intrinsic pathways. DCZ0805 suppressed the NF-κB signaling pathway activation, which may have contributed to the inhibition of cell proliferation. DCZ0805 treatment remarkably reduced the tumor burden in the immunocompromised xenograft mouse model, with no obvious toxicity observed. Conclusion The findings of this study indicate that DCZ0805 can serve as a novel therapeutic agent for the treatment of MM.

scholarly journals Gomisin M2 Ameliorates Atopic Dermatitis-like Skin Lesions via Inhibition of STAT1 and NF-κB Activation in 2,4-Dinitrochlorobenzene/Dermatophagoides farinae Extract-Induced BALB/c Mice

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4409
Author(s):  
Jinjoo Kang ◽  
Soyoung Lee ◽  
Namkyung Kim ◽  
Hima Dhakal ◽  
Taeg-Kyu Kwon ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Oral Administration ◽  
Skin Diseases ◽  
Nuclear Translocation ◽  
Skin Lesions ◽  
Biologically Active ◽  
Therapeutic Effects ◽  
Dermatophagoides Farinae ◽  
Tnf Α ◽  
Ifn Γ

The extracts of Schisandra chinensis (Turcz.) Baill. (Schisandraceae) have various therapeutic effects, including inflammation and allergy. In this study, gomisin M2 (GM2) was isolated from S. chinensis and its beneficial effects were assessed against atopic dermatitis (AD). We evaluated the therapeutic effects of GM2 on 2,4-dinitrochlorobenzene (DNCB) and Dermatophagoides farinae extract (DFE)-induced AD-like skin lesions with BALB/c mice ears and within the tumor necrosis factor (TNF)-α and interferon (IFN)-γ-stimulated keratinocytes. The oral administration of GM2 resulted in reduced epidermal and dermal thickness, infiltration of tissue eosinophils, mast cells, and helper T cells in AD-like lesions. GM2 suppressed the expression of IL-1β, IL-4, IL-5, IL-6, IL-12a, and TSLP in ear tissue and the expression of IFN-γ, IL-4, and IL-17A in auricular lymph nodes. GM2 also inhibited STAT1 and NF-κB phosphorylation in DNCB/DFE-induced AD-like lesions. The oral administration of GM2 reduced levels of IgE (DFE-specific and total) and IgG2a in the mice sera, as well as protein levels of IL-4, IL-6, and TSLP in ear tissues. In TNF-α/IFN-γ-stimulated keratinocytes, GM2 significantly inhibited IL-1β, IL-6, CXCL8, and CCL22 through the suppression of STAT1 phosphorylation and the nuclear translocation of NF-κB. Taken together, these results indicate that GM2 is a biologically active compound that exhibits inhibitory effects on skin inflammation and suggests that GM2 might serve as a remedy in inflammatory skin diseases, specifically on AD.

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