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Peroxisome Proliferator Activated Receptor gamma (PPARγ) Agonist Rosiglitazone Ameliorate Airway Inflammation by Inhibiting Toll-Like Receptor 2 (TLR2)/Nod-Like Receptor with Pyrin Domain Containing 3 (NLRP3) Inflammatory Corpuscle Activation in Asthmatic Mice.
- Source :
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Medical science monitor : international medical journal of experimental and clinical research [Med Sci Monit] 2018 Dec 13; Vol. 24, pp. 9045-9053. Date of Electronic Publication: 2018 Dec 13. - Publication Year :
- 2018
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Abstract
- BACKGROUND The purpose of this study was to explore the function and mechanism of peroxisome proliferator activated receptor agonist (PPARγ) in the toll-like receptor 2 (TLR2)/nod-like receptor with pyrin domain containing 3 (NLRP3) inflammatory corpuscle pathway of asthmatic mice. MATERIAL AND METHODS Eighteen female mice (C57) were randomly divided into 4 groups: the control group, the asthma model group challenged by ovalbumin (OVA), the rosiglitazone group, and the PPARγ agonist rosiglitazone treatment group. The infiltration of peribronchial inflammatory cells as well as the proliferation and mucus secretion of bronchial epithelial goblet cells were observed by hematoxylin and eosin and periodic acid-Schiff staining. Western blots were employed to detect the expression levels of TLR2, PPARγ, nuclear factor-kappa B (NF-kappaB), NLRP3, and ASC [apoptosis-associated speck-like protein containing C-terminal caspase recruitment domain [CARD]). RESULTS The number of inflammatory cells and eosinophils, and the levels of OVAs IgE, interleukin-4 (IL-4), and IL-13 were significantly higher in the C57 asthma group compared to the C57 control group and the treatment group (P<0.05). The infiltration of peribronchiolar inflammatory cells, wall thickening, goblet cell hyperplasia, and mucus secretion in the treatment group were all significantly decreased compared to those in the asthma group. PPARg expression in the treatment group was significantly higher compared to the asthma group and the control group (P<0.05). The protein expression levels of TLR2, NF-kappaB, NLRP3, and ASC were significantly lower compared to the asthma group but were higher compared to the control group (P<0.05). CONCLUSIONS PPARγ rosiglitazone ameliorates airway inflammation by inhibiting NF-kappaB expression in asthmatic mice, and further inhibits the activation of TLR2/NLRP3 inflammatory corpuscles.
- Subjects :
- Animals
CARD Signaling Adaptor Proteins metabolism
Disease Models, Animal
Female
Inflammation metabolism
Mice
Mice, Inbred C57BL
NF-kappa B metabolism
NLR Family, Pyrin Domain-Containing 3 Protein metabolism
PPAR gamma metabolism
Signal Transduction drug effects
Thiazolidinediones metabolism
Toll-Like Receptor 2 metabolism
Asthma drug therapy
PPAR gamma antagonists & inhibitors
Rosiglitazone pharmacology
Toll-Like Receptor 2 antagonists & inhibitors
Subjects
Details
- Language :
- English
- ISSN :
- 1643-3750
- Volume :
- 24
- Database :
- MEDLINE
- Journal :
- Medical science monitor : international medical journal of experimental and clinical research
- Publication Type :
- Academic Journal
- Accession number :
- 30544130
- Full Text :
- https://doi.org/10.12659/MSM.910766