Anti-Inflammatory Effect of Artemisia argyi on Ethanol-Induced Gastric Ulcer: Analytical, In Vitro and In Vivo Studies for the Identification of Action Mechanism and Active Compounds.
Myoung-Sook ShinJaemin LeeJin Woo LeeSe Hoon ParkIl Kyun LeeJung A ChoiJung Suk LeeKi Sung KangPublished in: Plants (Basel, Switzerland) (2021)
Artemisia argyi is widely used as traditional medicine in East Asia. However, its effects against inflammation and gastric ulcers have not been reported yet. We analyzed anti-inflammatory activity and its molecular mechanisms of A. argyi using RAW264.7 cells line, then evaluated the curative efficacy in rats with acute gastric ulcers. Nitric oxide and IL-6 production was measured using Griess reagent and an ELISA kit. Inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and mucin (MUC)1, MUC5AC, and MUC6 mRNA were determined by SYBR Green or Taqman qRT-PCR methods. The phosphorylation of ERK, JNK, p38, and c-Jun protein were detected by western blotting. RW0117 inhibited LPS-induced NO and IL-6 production. The mRNA levels of iNOS and IL-6 were strongly suppressed. The phosphorylation of ERK, JNK, and c-Jun decreased by treatment with RW0117. Oral administration of RW0117 recovered the amount of mucin mRNA and protein level that was decreased due to gastric ulcers by HCl-EtOH. A. argyi exhibited strong anti-inflammatory effects and contributed to the modulation of HCl-EtOH-induced gastric ulcer in rats.
Keyphrases
- nitric oxide synthase
- nitric oxide
- signaling pathway
- lps induced
- induced apoptosis
- binding protein
- drug induced
- high glucose
- anti inflammatory
- cell death
- inflammatory response
- diabetic rats
- cell proliferation
- oxidative stress
- pi k akt
- hydrogen peroxide
- endoplasmic reticulum stress
- liver failure
- cell cycle arrest
- rectal cancer
- wound healing
- combination therapy