Korean J Physiol Pharmacol.  2009 Aug;13(4):295-300. 10.4196/kjpp.2009.13.4.295.

The Inhibitory Effect of Quercetin-3-O-beta-D-Glucuronopyranoside on Gastritis and Reflux Esophagitis in Rats

• Min YS
• Lee SE
• Hong ST
• Kim HS
• Choi BC
• Sim SS
• Whang WK
• Sohn UD

• KMID: 2071684
• DOI: http://doi.org/10.4196/kjpp.2009.13.4.295

Abstract

It was evaluated the inhibitory action of quercetin-3-O-beta-D-glucuronopyranoside (QGC) on reflux esophagitis and gastritis in rats. QGC was isolated from the herba of Rumex Aquaticus. Reflux esophagitis or gastritis was induced surgically or by administering indomethacin, respectively. Oral QGC decreased ulcer index, injury area, gastric volume, and acid output and increased gastric pH as compared with quercetin. Furthermore, QGC significantly decreased gastric lesion sizes induced by exposing the gastric mucosa to indomethacin. Malondialdehyde levels were found to increase significantly after inducing reflux esophagitis, and were reduced by QGC, but not by quercetin or omeprazole. These results show that QGC can inhibit reflux esophagitis and gastritis in rats.

Keyword

Reflux esophagitis; Lipid peroxidation; Gastritis; Quercetin-3-O-beta-D-glucuronopyranoside

MeSH Terms

Animals
Esophagitis, Peptic
Gastric Mucosa
Gastritis
Hydrogen-Ion Concentration
Indomethacin
Lipid Peroxidation
Malondialdehyde
Omeprazole
Quercetin
Rats
Rumex
Ulcer
Indomethacin
Malondialdehyde
Omeprazole
Quercetin

Figure

• 

  Fig. 1. The effect of QGC on reflux esophagitis induced surgically in rats. Mean lesion area in the control group was 4 (0, no lesion; 1, ulcer area; 2, ulcer area <30 mm2; 3, ulcer area >30 mm2; 4, complete lesion (perforation of the esophageal mucosa). QGC treated animals showed significantly inhibition on reflux esophagitis. Data are means±SEMs of 6~8 animals. ∗Significantly different from the corresponding controls. ∗p<0.05, ∗∗p<0.01, and ∗∗∗p< 0.001 vs. the control.

• 

  Fig. 2. The effect of QGC on gastric volume. QGC significantly and dose-dependently decreased gastric volume. Data are means±SEM. ∗p<0.05, ∗∗p<0.01, and ∗∗∗p<0.001 vs. the control (n=6~8).

• 

  Fig. 3. The effects of QGC on gastric pH. QGC administration changed the pH of reflux esophagitis in rats. QGC significantly increased when compared with the pH of quercetin. Data are means±SEM. ∗p<0.05, ∗∗∗p<0.001 vs. the control (n=6~8).

• 

  Fig. 4. The inhibitory effect of QGC on gastric acid output. QGC significantly increased when compared to the acidity of quercetin. Data are means±SEM. ∗Significantly different from the corresponding control. ∗p<0.05, ∗∗p<0.01, and ∗∗∗p<0.001 vs. the control (n=6~8).

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  Fig. 5. The inhibitory effects of QGC on lipid peroxidation. In the gastritis control group levels of lipid peroxidation were elevated as compared with the normal group. QGC administration significantly decreased the amount of MDA formation, suggesting that it inhibited gastritis induced lipid peroxidation. Column represent means±SEMs of 6~8 animals. ∗p<0.05 and ∗∗p<0.01 vs. control.

• 

  Fig. 6. The inhibitory effect of QGC on indomethacin-induced gastritis. Mean lesion area in the control group was 4.0±0.7 cm2. QGC (0.001~0.01 mg/kg, p.o.) dose-dependently inhibited the formation of indomethacin-induced lesions. Data are means±SEM of 6~8 animals. ∗Significantly different from the corresponding control. ∗p<0.05 and ∗∗∗p<0.001 vs control.

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