Adropin attenuates pancreatitisassociated lung injury through PPARγ phosphorylationrelated macrophage polarization.
Int J Mol Med
; 52(4)2023 10.
Article
en En
| MEDLINE
| ID: mdl-37654184
ABSTRACT
Acute pancreatitis (AP)associated lung injury (ALI) is a critical complication of AP. Adropin is a regulatory protein of immune metabolism. The present study aimed to explore the immunomodulatory effects of adropin on APALI. For this purpose, serum samples of patients with AP were collected and the expression levels of serum adropin were detected using ELISA. Animal models of AP and adropin knockout (AdroKO) were constructed, and adropin expression in serum and lung tissues was investigated. The levels of fibrosis and apoptosis were evaluated using hematoxylin and eosin staining, Masson's staining and immunohistochemistry of in lung tissue. M1/M2 type macrophages in the lungs were detected using immunofluorescence staining, western blot analysis and reverse transcriptionquantitative PCR. As shown by the results, adropin expression was decreased in AP. In the AdroKO + Larginine (LArg) group, macrophage infiltration, fibrosis and apoptosis were increased. The expression of peroxisome proliferator activated receptor γ (PPARγ) was downregulated, and the macrophages exhibited a trend towards M1 polarization in the AdroKO + LArg group. Adropin exogenous supplement attenuated the levels of fibrosis and apoptosis in the model of AP. Adropin exogenous supplement also increased PPARγ expression by the regulation of the phosphorylation levels, which was associated with M2 macrophage polarization. On the whole, the findings of the present study suggest that adropin promotes the M2 polarization of lung macrophages and reduces the severity of APALI by regulating the function of PPARγ through the regulation of its phosphorylation level.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Lesión Pulmonar
/
Macrófagos
Tipo de estudio:
Etiology_studies
/
Prognostic_studies
/
Risk_factors_studies
Límite:
Animals
Idioma:
En
Revista:
Int J Mol Med
Asunto de la revista:
BIOLOGIA MOLECULAR
/
GENETICA MEDICA
Año:
2023
Tipo del documento:
Article