Premium
Plant‐originated extract of Cucurbita Maxim Sweet prevents foregut damage induced by entero‐salivary nitrites recirculation impair via suppression of inflammatory mediators’ expression
Author(s) -
PshykTitko Irena,
Zajachkivska Oksana,
Yashchenko Antonina
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1168.5
Subject(s) - foregut , pharmacology , chemistry , biology , anatomy
Cucurbita maxim sweet seed extract (CSE), Ukrainian plant hybrid kavbuz from watermelon and pumpkin, contents high amount of beta‐carotene and bioflavonoids. Studies in vitro showed that CSE exhibits a variety of actions via antioxidant and vasotropic effects, yet the mechanism remains still unknown. In this study, to investigate the mechanism responsible for these actions, we examined the effect of CSE on changes in inflammatory mediator's expression in foregut during modeling of entero‐salivary nitrites recirculation (mESNR), an important functional cytoprotective system in foregut. Rats were used with dose‐depended treatment without/with CSE in dose 50–200 mg/kg under mESNR by acid blocks atropine (3 mg/kg), ranitidine (100 mg/kg), L‐NAME (10 mg/kg) and their combination; oral, esophageal, gastric lesions were determined by histology score index (HIS); IL‐1beta, IL‐8 via ELISA. ESNR impairment caused nonerosive hemorrhagic lesions in foregut mucosa, as well as dystrophic changes in muscular layer, accompanied by increased IL‐1beta, IL‐8 syntesis.CSE potently prevented cytolytic response to changes of ESNR, with concomitant decreasing of IL‐1beta, IL‐8; these effects of CSE were significantly abrogated by pretreatment of L‐NAME. CSE prevents mESNR‐induced foregut lesions via suppression of inflammatory mediators such as IL‐1beta, IL‐8, the important pathogenic factors in foregut.