PMID- 37954373
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231114
IS  - 2405-8440 (Print)
IS  - 2405-8440 (Electronic)
IS  - 2405-8440 (Linking)
VI  - 9
IP  - 11
DP  - 2023 Nov
TI  - Atractylenolide III ameliorated reflux esophagitis via PI3K/AKT/NF-kappaB/iNOS 
      pathway in rats.
PG  - e21224
LID - 10.1016/j.heliyon.2023.e21224 [doi]
LID - e21224
AB  - Reflux esophagitis (RE), an esophageal inflammation caused by reflux of gastric 
      contents, often damages the lower esophagus, seriously affecting the quality of 
      life of patients. This study aims to investigate the therapeutic effects and 
      underlying molecular mechanisms of atractylenolide III (ATL III) on RE model 
      rats. In this research, the RE rat model is established sequentially following 
      hemipyloric ligation, cardia transection, and hydrochloric acid perfusion. 
      Further, the RE-induced rats are intragastrically administrated with ATL III 
      (0.6, 1.2, and 2.4 mg/kg/D) for 28 days to evaluate ATL III therapeutic effects. 
      To study the molecular mechanism, RE rats are treated with a phosphoinositide-3 
      kinase (PI3K) agonist (740 Y-P) combined with ATL III. The histopathological 
      changes in the esophagus are eventually observed by hematoxylin & eosin (H&E) 
      staining. In addition to changes in gastric pH and levels of reactive oxygen 
      species (ROS), enzyme-linked immunosorbent assay (ELISA) and Western blot 
      analyses are used to detect the expression levels of tumor necrosis factor-alpha 
      (TNF-alpha, mmol/L), interleukin (IL)-8, IL-6, IL-1beta in the esophageal tissues. As a 
      result, the lesions in the esophageal tissues of RE rats are alleviated, 
      decreasing the macroscopic observation scores of the esophageal mucosa after ATL 
      III treatment,. The experimental results indicated significantly increased pH 
      value of the gastric contents and reduced ROS, thiobarbituric acid reactants 
      (TBARS), TNF-alpha, IL-8, IL-6, and IL-1beta levels, as well as expression levels of 
      p-PI3K, p-AKT, iNOS, and nuclear NF-kappaB proteins in esophageal tissues. In 
      conclusion, the study indicated that ATL III could efficiently treat RE in rats 
      by inhibiting oxidative stress and inflammatory damage through the 
      PI3K/AKT/NF-kappaB/iNOS pathway.
CI  - (c) 2023 Published by Elsevier Ltd.
FAU - Si, Xianzhe
AU  - Si X
AD  - Department of Gastrointestinal & Esophageal Surgery, The 2nd Affiliated Hospital 
      of Fujian Medical University, Quanzhou, China.
FAU - Lin, Weijie
AU  - Lin W
AD  - Department of Gastrointestinal & Esophageal Surgery, The 2nd Affiliated Hospital 
      of Fujian Medical University, Quanzhou, China.
FAU - Chen, Zhiyao
AU  - Chen Z
AD  - Department of Gastrointestinal & Esophageal Surgery, The 2nd Affiliated Hospital 
      of Fujian Medical University, Quanzhou, China.
FAU - Xu, Jie
AU  - Xu J
AD  - Department of Gastrointestinal & Esophageal Surgery, The 2nd Affiliated Hospital 
      of Fujian Medical University, Quanzhou, China.
FAU - Huang, Wenbo
AU  - Huang W
AD  - Department of Gastrointestinal & Esophageal Surgery, The 2nd Affiliated Hospital 
      of Fujian Medical University, Quanzhou, China.
FAU - Chen, Feng
AU  - Chen F
AD  - Department of Gastrointestinal & Esophageal Surgery, The 2nd Affiliated Hospital 
      of Fujian Medical University, Quanzhou, China.
FAU - Lin, Jianqing
AU  - Lin J
AD  - Department of Oncology, The 2nd Affiliated Hospital of Fujian Medical University, 
      Quanzhou, China.
FAU - Huang, Zhijun
AU  - Huang Z
AD  - Department of Gastrointestinal & Esophageal Surgery, The 2nd Affiliated Hospital 
      of Fujian Medical University, Quanzhou, China.
LA  - eng
PT  - Journal Article
DEP - 20231023
PL  - England
TA  - Heliyon
JT  - Heliyon
JID - 101672560
PMC - PMC10632696
OTO - NOTNLM
OT  - Atractylenolide III
OT  - PI3K/AKT/NF-kappaB/iNOS pathway
OT  - Rats
OT  - Reflux esophagitis
COIS- This research did not receive any specific grant from funding agencies in the 
      public, commercial, or not-for-profit sectors.
EDAT- 2023/11/13 06:43
MHDA- 2023/11/13 06:44
PMCR- 2023/10/23
CRDT- 2023/11/13 04:28
PHST- 2023/06/05 00:00 [received]
PHST- 2023/09/17 00:00 [revised]
PHST- 2023/10/18 00:00 [accepted]
PHST- 2023/11/13 06:44 [medline]
PHST- 2023/11/13 06:43 [pubmed]
PHST- 2023/11/13 04:28 [entrez]
PHST- 2023/10/23 00:00 [pmc-release]
AID - S2405-8440(23)08432-3 [pii]
AID - e21224 [pii]
AID - 10.1016/j.heliyon.2023.e21224 [doi]
PST - epublish
SO  - Heliyon. 2023 Oct 23;9(11):e21224. doi: 10.1016/j.heliyon.2023.e21224. 
      eCollection 2023 Nov.