-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Ades adit detitis (AD) is a chronic inflammatory skin disease characterized by skin barrier defects and Th2 immune response.
shell protease 3-like 1 (CHI3L1), also known as mammary regression protein 39 (BRP-39) and human YKL-40, play an important role in Th2 inflammation and allergen sensitivity.
CHI3L1 is involved in a variety of diseases, including asthma characterized by inflammation, apoptosis and tissue remodeling, but its role in AD is not yet known.
study, which explores the role of CHI3L1 in the occurrence and progress of AD, was published online in Clin Oral Investig.
we investigated the levels of YKL-40 in the serum and skin of AD patients, respectively, using ELISA and immunofluorescence.
The AD model of mice induced by egg white protein (OVA) was studied in mice with wild type (WT) and BRP-39 invalid mutation (BRP-39-/-) to study Th2 immune response, M2 macrophage activity and skin barrier gene expression.
results showed a significant increase in YKL-40 levels in the serum of AD patients.
, the mRNA and protein expression levels of BLP-39 were higher in OVA-sensitive WT mice than in control mice.
OVA-sensitive BLP-39-/- mice had lower skin thickness, serum total IgE, Th2 cytokine levels, and cd4-effect T-cell count than OVA-sensitive WT mice.
BLP-39 is dominant in leather macrophages.
BLP-39 is involved in the activation of M2 macrophages.
same, YKL-40 levels in the skin of AD patients were higher than normal and expressed in dermatocy macrophages.
the absence of BLP-39 reduces the imbalance between the skin barrier and the tightening gene.
, these results show that CHI3L1 mediates the development of OVA-induced AD, affecting Th2 inflammation, M2 macrophage activity, and skin barrier function.
.