Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2005 Nov 14;11(42):6662-6.
doi: 10.3748/wjg.v11.i42.6662.

Gastroprotective activity of Nigella sativa L oil and its constituent, thymoquinone against acute alcohol-induced gastric mucosal injury in rats

Mehmet Kanter  1 , Halit Demir, Cengiz Karakaya, Hanefi Ozbek
Affiliations

Gastroprotective activity of Nigella sativa L oil and its constituent, thymoquinone against acute alcohol-induced gastric mucosal injury in rats

Mehmet Kanter et al. World J Gastroenterol. .

Abstract

Aim: To evaluate the role of reactive oxygen species in the pathogenesis of acute ethanol-induced gastric mucosal lesions and the effect of Nigella sativa L oil (NS) and its constituent thymoquinone (TQ) in an experimental model.

Methods: Male Wistar albino rats were assigned into 4 groups. Control group was given physiologic saline orally (10 mL/kg body weight) as the vehicle (gavage); ethanol group was administrated 1 mL (per rat) absolute alcohol by gavage; the third and fourth groups were given NS (10 mL/kg body weight) and TQ (10 mg/kg body weight p.o) respectively 1 h prior to alcohol intake. One hour after ethanol administration, stomach tissues were excised for macroscopic examination and biochemical analysis.

Results: NS and TQ could protect gastric mucosa against the injurious effect of absolute alcohol and promote ulcer healing as evidenced from the ulcer index (UI) values. NS prevented alcohol-induced increase in thiobarbituric acid-reactive substances (TBARS), an index of lipid peroxidation. NS also increased gastric glutathione content (GSH), enzymatic activities of gastric superoxide dismutase (SOD) and glutathione-S-transferase (GST). Likewise, TQ protected against the ulcerating effect of alcohol and mitigated most of the biochemical adverse effects induced by alcohol in gastric mucosa, but to a lesser extent than NS. Neither NS nor TQ affected catalase activity in gastric tissue.

Conclusion: Both NS and TQ, particularly NS can partly protect gastric mucosa from acute alcohol-induced mucosal injury, and these gastroprotective effects might be induced, at least partly by their radical scavenging activity.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Mean UI in ethanol, ethanol + NS and ethanol + TQ treated rats. bP<0.01, aP<0.05 vs ethanol group
See this image and copyright information in PMC

References

    1. Szabo S, Trier JS, Frankel PW. Sulfhydryl compounds may mediate gastric cytoprotection. Science. 1981;214:200–202. - PubMed
    1. Cho CH, Pfeiffer CJ, Misra HP. Ulcerogenic mechanism of ethanol and the action of sulphanilyl fluoride on the rat stomach in-vivo. J Pharm Pharmacol. 1991;43:495–498. - PubMed
    1. Lutnicki K, Wróbel J, Ledwozyw A, Trebas-Pietraś E. The effect of calcium ions on the intensity of peroxidation processes and the severity of ethanol-induced injury to the rat's gastric mucosa. Arch Vet Pol. 1992;32:125–132. - PubMed
    1. Bast A, Haenen GR, Doelman CJ. Oxidants and antioxidants: state of the art. Am J Med. 1991;91:2S–13S. - PubMed
    1. Hirokawa M, Miura S, Yoshida H, Kurose I, Shigematsu T, Hokari R, Higuchi H, Watanabe N, Yokoyama Y, Kimura H, et al. Oxidative stress and mitochondrial damage precedes gastric mucosal cell death induced by ethanol administration. Alcohol Clin Exp Res. 1998;22:111S–114S. - PubMed

MeSH terms