Spiraea prunifolia var. simpliciflora Attenuates Oxidative Stress and Inflammatory Responses in a Murine Model of Lipopolysaccharide-Induced Acute Lung Injury and TNF-α-Stimulated NCI-H292 Cells.
Ba-Wool LeeJi-Hye HaHan-Gyo ShinSeong-Hun JeongDa-Bin JeonJu-Hong KimJi-Young ParkHyung-Jun KwonKyungsook JungWoo-Song LeeHyeon-Young KimSung-Hwan KimHyun-Jae JangYoung-Bae RyuIn-Chul LeePublished in: Antioxidants (Basel, Switzerland) (2020)
Spiraea prunifolia var. simpliciflora (SP) is traditionally used as an herbal remedy to treat fever, malaria, and emesis. This study aimed to evaluate the anti-oxidative and anti-inflammatory properties of the methanol extract of SP leaves in tumor necrosis factor (TNF)-α-stimulated NCI-H292 cells and in a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. SP decreased the number of inflammatory cells and the levels of TNF-α, interleukin (IL)-1β, and IL-6 in the bronchoalveolar lavage fluid, and inflammatory cell infiltration in the lung tissues of SP-treated mice. In addition, SP significantly suppressed the mRNA and protein levels of TNF-α, IL-1β, and IL-6 in TNF-α-stimulated NCI-H292 cells. SP significantly suppressed the phosphorylation of the mitogen-activated protein kinases (MAPKs) and p65-nuclear factor-kappa B (NF-κB) in LPS-induced ALI mice and TNF-α-stimulated NCI-H292 cells. SP treatment enhanced the nuclear translocation of nuclear factor erythroid 2-related factor (Nrf2) with upregulated antioxidant enzymes and suppressed reactive oxygen species (ROS)-mediated oxidative stress in the lung tissues of LPS-induced ALI model and TNF-α-stimulated NCI-H292 cells. Collectively, SP effectively inhibited airway inflammation and ROS-mediated oxidative stress, which was closely related to its ability to induce activation of Nrf2 and inhibit the phosphorylation of MAPKs and NF-κB. These findings suggest that SP has therapeutic potential for the treatment of ALI.
Keyphrases
- lps induced
- oxidative stress
- induced apoptosis
- inflammatory response
- nuclear factor
- lipopolysaccharide induced
- rheumatoid arthritis
- toll like receptor
- cell cycle arrest
- dna damage
- endoplasmic reticulum stress
- mouse model
- signaling pathway
- reactive oxygen species
- anti inflammatory
- stem cells
- cell death
- type diabetes
- gene expression
- single cell
- metabolic syndrome
- cell therapy
- insulin resistance
- bone marrow
- diabetic rats
- mesenchymal stem cells
- replacement therapy