p-Coumaric Acid Attenuates Lipopolysaccharide-Induced Lung Inflammation in Rats by Scavenging ROS Production: an In Vivo and In Vitro Study.
Maryam KheiryMahin DianatMohammad BadaviSeyyed Ali MardVahid BayatiPublished in: Inflammation (2020)
Lipopolysaccharide (LPS), known as lipoglycans and endotoxins found in the cell wall of some type of Gram-negative bacteria, causes acute lung inflammation (ALI). p-Coumaric acid (p-CA) possesses anti-inflammatory and anti-oxidative activities. The main purpose of our research was to explore the effect of p-CA on LPS-induced inflammation. In part I, 32 rats were divided into four groups: Control, LPS (5 mg/kg), p-CA (100 mg/kg), and LPS + p-CA to investigate acute lung inflammation caused by LPS. In part II, the effect of LPS-stimulated inflammatory response on A549 cells was investigated. The dosage of LPS and p-CA which used in this part was 1 μg/ml and 20 mM, respectively. ALI rats showed an elevation in antioxidant activity, TNF-alpha, IL-6, MDA, inflammatory parameters, and Nrf2 gene expression. Although pre-treatment with p-CA could return these changes approximately to normal condition in all two-part studies (in vivo and in vitro). The results of in vivo and in vitro study showed that LPS induced lung inflammation. Pre-treatment with p-CA causes modulating of oxidative stress in inflammatory condition in lung injury and A549 cell.
Keyphrases
- inflammatory response
- lps induced
- oxidative stress
- lipopolysaccharide induced
- induced apoptosis
- toll like receptor
- anti inflammatory
- gene expression
- dna damage
- protein kinase
- diabetic rats
- ischemia reperfusion injury
- dna methylation
- rheumatoid arthritis
- cell proliferation
- single cell
- high resolution
- respiratory failure
- combination therapy
- cell death
- breast cancer cells
- cell cycle arrest
- intensive care unit
- acute respiratory distress syndrome
- heat shock
- mass spectrometry
- immune response
- aortic dissection
- reactive oxygen species
- smoking cessation
- bone marrow