Sorbaria kirilowii Ethanol Extract Exerts Anti-Inflammatory Effects In Vitro and In Vivo by Targeting Src/Nuclear Factor (NF)-κB.
Jiwon JangJong Sub LeeYoung-Jin JangEui Su ChoungWan Yi LiSang Woo LeeEunji KimJong-Hoon KimYoung-Jin SonPublished in: Biomolecules (2020)
Inflammation is a fundamental process for defending against foreign antigens that involves various transcriptional regulatory processes as well as molecular signaling pathways. Despite its protective roles in the human body, the activation of inflammation may also convey various diseases including autoimmune disease and cancer. Sorbaria kirilowii is a plant originating from Asia, with no anti-inflammatory activity reported. In this paper, we discovered an anti-inflammatory effect of S. kirilowii ethanol extract (Sk-EE) both in vivo and in vitro. In vitro effects of Sk-EE were determined with lipopolysaccharide (LPS)-stimulated RAW264.7 cells, while ex vivo analysis was performed using peritoneal macrophages of thioglycollate (TG)-induced mice. Sk-EE significantly reduced the nitric oxide (NO) production of induced macrophages and inhibited the expression of inflammation-related cytokines and the activation of transcription factors. Moreover, treatment with Sk-EE also decreased the activation of proteins involved in nuclear factor (NF)-κB signaling cascade; among them, Src was a prime target of Sk-EE. For in vivo assessment of the anti-inflammatory effect of Sk-EE, HCl/EtOH was given by the oral route to mice for gastritis induction. Sk-EE injection dose-dependently reduced the inflammatory lesion area of the stomach in gastritis-induced mice. Taking these results together, Sk-EE exerts its anti-inflammatory activity by regulating intracellular NF-κB signaling pathways and also shows an authentic effect on reducing gastric inflammation.
Keyphrases
- nuclear factor
- oxidative stress
- diabetic rats
- anti inflammatory
- toll like receptor
- signaling pathway
- induced apoptosis
- high glucose
- transcription factor
- nitric oxide
- pi k akt
- lps induced
- inflammatory response
- endothelial cells
- drug induced
- helicobacter pylori
- high fat diet induced
- tyrosine kinase
- squamous cell carcinoma
- epithelial mesenchymal transition
- poor prognosis
- dendritic cells
- multiple sclerosis
- helicobacter pylori infection
- cell proliferation
- papillary thyroid
- metabolic syndrome
- long non coding rna
- young adults
- hydrogen peroxide
- combination therapy
- squamous cell
- childhood cancer