[논문]Anti-Oxidative and Anti-Inflammatory Effects of QGC in Cultured Feline Esophageal Epithelial Cells

Lee, Myeong Jae; Song, Hyun Ju; Jeong, Jun Yeong; Park, Sun Young; Sohn, Uy Dong

doi:10.4196/kjpp.2013.17.1.81

Anti-Oxidative and Anti-Inflammatory Effects of QGC in Cultured Feline Esophageal Epithelial Cells 원문보기

The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, v.17 no.1, 2013년, pp.81 - 87

Lee, Myeong Jae (Department of Pharmacology, College of Pharmacy, Chung-Ang University) , Song, Hyun Ju (Department of Pharmacology, College of Pharmacy, Chung-Ang University) , Jeong, Jun Yeong (Department of Pharmacology, College of Pharmacy, Chung-Ang University) , Park, Sun Young (Department of Pharmacology, College of Pharmacy, Chung-Ang University) , Sohn, Uy Dong (Department of Pharmacology, College of Pharmacy, Chung-Ang University)

Abstract ▼ AI-Helper

Quercetin-3-O-${\beta}$-D-glucuronopyranoside (QGC) is a flavonoid glucoside extracted from Rumex Aquaticus Herba. In the present study, anti-oxidative and anti-inflammatory effects of QGC were tested in vitro. Epithelial cells obtained from cat esophagus were cultured. When the cells were exposed to acid for 2 h, cell viability was decreased to 36%. Pretreatment with 50 ${\mu}M$ QGC for 2 h prevented the reduction in cell viability. QGC also inhibited the productions of intracellular ROS by inflammatory inducers such as acid, lipopolysaccharide, indomethacin and ethanol. QGC significantly increased the activities of superoxide dismutase (SOD) and catalase, and also induced the expression of SOD2, while it restored the decrease of catalase expression in cells exposed to acid. QGC inhibited NF-${\kappa}B$ translocation, cyclooxygenase-2 expression and $PGE_2$ secretion in cells exposed to acid, which plays an important role in the pathogenesis of esophagitis. The data suggest that QGC may well be one of the promising substances to attenuate oxidative epithelial cell injury and inflammatory signaling in esophagus inflammation.

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가설 설정

First, we assessed whether QGC itself has any effect on cell viability in cultured EECs. Serum-starved cells were incubated with the given concentration of QGC for the indicated time.

제안 방법

For experiments designed to measure the release of PGE2 due to endogenous arachidonic acid, the medium was collected, centrifuged, and stored at –70℃ until assay.

데이터처리

Data are expressed as means±SEM of separate experiments and the statistical differences between means were determined by Student’s t-test.

이론/모형

1. Cell viability evaluated by MTT assay. (A) Effect of QGC on cell viability of esophageal epithelial cells.
Cell viability was determined by the conventional MTT reduction assay. Viable cells convert MTT to insoluble blue formazan crystals by mitochondrial respiratory chain enzyme succinate dehydrogenase.
Serum-starved EECs were pre-incubated with the presence of 50 μM QGC for 2 h. Cells were then stimulated with the indicated inflammatory inducers and their ROS production was estimated using DCF-DA assay (Fig. 2). Inflammatory inducers including acid (pH 4 medium, 10 min), LPS (1 μM/ml, 15 h), indomethacin (2 mM, 2 h) and ethanol (10%, 1 h) induced significant increases in ROS production by 138.
Cells were then stimulated with the indicated inflammatory inducers: (A) pH 4 medium for 10 min (B) 1 μM/ml LPS 15 h (C) 2 mM indomethacin for 2 h and (D) 10% ethanol for 1 h. ROS production was estimated using DCF-DA assay. Data are expressed as means±SEM of three experiments (Student’s t-test: *p ＜0.

성능/효과

In conclusion, our data suggest that QGC exhibits potent down regulation of ROS generation and protective activity against acid-induced cell damage in EECs. QGC exerts the anti-oxidative effect through the expression of SOD and catalase as well as their activation.

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