Method for inhibiting occurrence of psoriasis by adopting tryptophan metabolite

A technology for psoriasis and tryptophan, applied in drug combination, skin diseases, drug delivery, etc., can solve problems such as hindering the treatment plan of psoriasis, hindering the interaction between skin microbiota and the host, etc., and achieve good medicinal prospects , the effect of inhibiting the onset of psoriasis and inhibiting the expression of cytokines

Pending Publication Date: 2021-11-26
AIR FORCE MEDICAL UNIV
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  • Application Information

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Problems solved by technology

However, most of these studies have focused on changes in bacterial abundance between psoriatic lesions and healthy skin, and the metabolism of the skin microbiota remains largely unknown, hindering insights into the functional importance of skin microbiota-host interactions. A comprehensive understanding, especially of the regulatory relationship between skin microbiota metabolism and the NLRP3 inflammasome, has also hampered progress in the development of novel psoriasis therapeutics beyond conventional technologies

Method used

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  • Method for inhibiting occurrence of psoriasis by adopting tryptophan metabolite
  • Method for inhibiting occurrence of psoriasis by adopting tryptophan metabolite
  • Method for inhibiting occurrence of psoriasis by adopting tryptophan metabolite

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0021] Example 1: QA levels in psoriasis patients' skin lesions and non-skin lesions decrease

[0022] In order to verify that QA is involved in the pathogenesis of psoriasis, the level of QA was analyzed on the skin of psoriasis patients with skin lesions and non-lesions.

[0023] 1. Use the gel patch method to collect metabolites on the skin surface of healthy subjects (healthy skin) and psoriasis patients (skin lesions and non-skin lesions) to obtain skin surface microbiota samples;

[0024] 2. Use liquid chromatography-tandem mass spectrometry to analyze and compare the levels of Trp metabolites on the skin surface of psoriasis patients and healthy subjects;

[0025] The result obtained is as figure 1 As shown, the conclusions are as follows:

[0026] Among the Trp level metabolites, QA was significantly lower in psoriasis patients in skin lesions (lesions) and non-lesions (nonlesions) than in healthy subjects. In addition, there was a significant negative linear correl...

Embodiment 2

[0027] Example 2: QA attenuates IMQ-induced psoriasiform dermatitis and inflammatory cell infiltration in mice

[0028] Based on the experiment in Example 1, QA is used to inhibit the onset of psoriasis and reduce the infiltration of inflammatory cells. Experiments were performed using a conventional IMQ-induced psoriasis-like mouse model.

[0029] Experimental group: smear IMQ on the ears of mice at a concentration of 5%, 25mg / ear / day. After smearing IMQ for 60 minutes, apply QA with a concentration of 10μg / ml (diluted in dimethyl sulfoxide) to the IMQ smearing place On the skin of the mouse, use it continuously for 7 days, and observe the skin of the mouse where the drug is applied on the 5th and 7th day;

[0030] Control group: IMQ was used alone on the ears of mice, at a concentration of 5%, 25 mg / ear / day, for 7 consecutive days, and the skin of the mice where the drug was applied was observed on the 5th and 7th days.

[0031] The result obtained is as figure 2 As show...

Embodiment 3

[0038] Example 3: Activation of Aryl Hydrocarbon Receptor AhR Inhibition of NLRP3 Inflammasome Inhibition of Psoriasis

[0039] Based on the above examples, it is verified that the use of QA to inhibit the onset of psoriasis is effective, but how QA inhibits the NLRP3 inflammasome still needs to be further explored.

[0040] HaCaT cells were cultured according to the existing technology, and after the keratinocytes were treated with QA at a concentration of 100 μg / mL, the results were as follows Figure 4 Shown: The results showed that QA-treated keratinocytes exhibited significantly increased mRNA and protein levels of AhR and CYP1A1 (the main downstream molecules of AhR activation), suggesting that AhR signaling is activated by QA in keratinocytes, further immunofluorescence data confirmed this result.

[0041]Simultaneously, small interfering RNA was used to interfere with AhR expression in keratinocytes, and then mixed inflammatory cytokines were added to simulate an in v...

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Abstract

The invention discloses a method for inhibiting occurrence of psoriasis by adopting tryptophan metabolite, and belongs to the technical field of psoriasis treatment, the method adopts quinolinic acid to treat psoriasis, the quinolinic acid inhibits NLRP3 inflammasome to inhibit psoriasis by activating an aromatic hydrocarbon receptor AhR, and particularly, the metabolite quinolinic acid metabolized by tryptophan on the skin surface negatively regulates activation of an NLRP3 inflammasome pathway by activating AhR in a cell nucleus, so that secretion of inflammatory cytokines is inhibited to participate in attack of psoriasis.

Description

technical field [0001] The invention relates to the technical field of psoriasis treatment, in particular to a method for inhibiting the onset of psoriasis by using tryptophan metabolites. Background technique [0002] A large microbiota inhabits the skin, shares nutrients with the host, and produces metabolites involved in regulating skin health status and immune function. Tryptophan (Trp) metabolites produced by the microbiota have received extensive attention for their role in immune regulation, especially immunosuppression. Multiple studies have shown that they play a role in the maturation of immune tissue and the fine-tuning of inflammatory diseases such as inflammatory bowel disease, rheumatoid arthritis, metabolic syndrome, neuropsychiatric features, and others. Compared with the gut, the skin is in a dry, nutrient-poor, and acidic environment, so the metabolic functions of the skin microbiota are quite different from those of the gut. The stratum corneum of the ep...

Claims

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Application Information

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IPC IPC(8): A61K31/44A61K9/06A61K9/00A61P17/06
CPCA61K31/44A61K9/06A61K9/0014A61P17/06
Inventor 王刚乔佩党二乐
Owner AIR FORCE MEDICAL UNIV
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