ABHD2 deficiency aggravates ovalbumin-induced airway remodeling through the PI3K/Akt pathway in an animal model of chronic asthma

• Autorzy: Qiang L. , Li X. , Li Q. , Bo H. , Liu Y. , Lv M. , Chen X. , Ju H. , Sang X. , Li Z. , Jin S.
• Języki publikacji: EN

Abstrakty

EN

Airway remodeling is a major pathological characteristic of chronic obstructive pulmonary disease (COPD). This study aimed to investigate the effect of Abhd2 deficiency on ovalbumin (OVA)-induced airway remodeling and inflammation in vivo. Abhd2-deficient mice were used to establish an OVA-induced asthma model. Lung tissues were analyzed using hematoxylin and eosin (HE) staining, Masson staining, immunohistochemistry, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and western blotting were used to determine the role of Abhd2 in the regulation of OVA-induced airway remodeling and inflammation. Our findings revealed that the RNA expression of inflammatory factors, including IL-1β, IL-6, IL-4, and IL-13, was significantly increased in OVA-induced Abhd2Gt/Gt asthmatic mice. The expression of IFN-γ was decreased significantly in OVA-induced Abhd2Gt/Gt asthmatic mice. The protein expression of airway remodeling factors, including α-SMA, type I collagen, and Ki67, was also increased in OVA-induced Abhd2Gt/Gt asthmatic mice compared to that in OVA-induced wild-type (WT) mice. Additionally, Abhd2 deficiency promoted the expression of p-Akt in tissues of the asthma model. These results suggest that Abhd2 deficiency exacerbates airway remodeling and inflammation through the PI3K/Akt pathway in chronic asthma.

• Wydawca: -
• Czasopismo: Polish Journal of Veterinary Sciences
• Rocznik: 2023
• Tom: 26
• Numer: 4
• Opis fizyczny: p.635-646,fig.,ref.

Twórcy

autor

Qiang L.

• Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

autor

Li X.

• Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

autor

Li Q.

• Department of pulmonary diseases, Heilongjiang Academy of Traditional Chinese Medicine, 33# Xidazhi Street, Harbin 150036, Heilongjiang, China

autor

Bo H.

• Department of Intensive Care Unit, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

autor

Liu Y.

• Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

autor

Lv M.

• Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

autor

Chen X.

• Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

autor

Ju H.

• Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

autor

Sang X.

• Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

autor

Li Z.

• University of Tokyo, 3-8-1# Bunkyo ku, Tokyo 1130033, Tokyo, Japan

autor

Jin S.

• Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University, 37# Yiyuan Street, Harbin 150001, Heilongjiang, China

Identyfikatory

DOI

10.24425/pjvs.2023.148283