Abstract
In this study, a medicinal herbal plant, Sanguisorba officinalis, was examined and screened for anti-Helicobacter pylori (H. pylori) activity. Seventy percent ethanol was used for herbal extraction. For anti-H. pylori activity screening, inhibitory zone tests as an in vitro assay and in vivo study using a Mongolian gerbil (Meriones unguiculatus) model were performed. Also, the safety of herbal compounds was evaluated by animal study. As a result of inhibitory zone test, Sanguisorba officinalis extract demonstrated strong anti-H. pylori activities. Also, as results of in vivo animal studies, Sanguisorba officinalis extract demonstrated strong therapeutic effects against H. pylori infection according to the criteria of histological examination and rapid urease test. As results of the safety study, after 28 days treatment of the Sanguisorba officinalis extract, the animals were not detected any grossly and histological changes. These results demonstrate that it can be successfully cured against H. pylori infection and protected from H. pylori-induced pathology with Sanguisorba officinalis extract. It could be a promising candidate herb treatment for patients with gastric complaints including gastric ulcer caused by H. pylori.
REFERENCES
An B. J.., Lee J. T.., Lee S. A.., Kwak J. H.., Park J. M.., Lee J. Y.., Son J. H.2004. Antioxidant effects and application as natural ingredients of Korean Sanguisorbae officinalis L. J. Korean Soc. Appl. Biol. Chem. 47(2):244–250.
Ahn Y. O.., Park B. J.., Yoo K. Y.., Kim N. K.., Heo D. S.., Lee J. K.., Ahn H. S.., Kang D. H.., Kim H.., Lee M.S.., Park T.S.1991. Incidence estimation of stomach cancer among Koreans. J. Kor. Med. Sci. 6:7–14.
Bastow K. F.., Bori I. D.., Fukushima Y.., Kashiwada Y.., Tanaka T.., Nonaka G.., Nishioka I.., Lee K.-H.1993. Inhibition of DNA Topoisomerases by sanguiin H-6, a cytotoxic dimeric ellagitannin from Sanguisorba officinalis. Planta Med. 59:240–245.
Han D.S.2007. Treatment of H. pylori infection and current status of vaccine development. Hanyang Med. Rev. 27:81–95.
Hansson L. E.., Nyren O.., Hsing A. W.., Bergstrom R.., Josefsson S.., Chow W. H.., Fraumeni J. F.., Adami H.O.1996. The risk of stomach cancer in patients with gastric or duodenal ulcer disease. N. Engl. J. Med. 355:242–249.
Harris A.1997. Treatment of Helicobacter pylori. Drugs Today. 33:59–66.
Honda S.., Fujioka T.., Tokieda M.., Satoh R.., Nishizono A.., Nasu M.1998. Development of Helicobacter pylori induced-gastric carcinoma in Mongolian gerbils. Cancer Res. 58:4255–4259.
Jung T. S.., Kang S. C.., Choi Y. J.., Jeon B. S.., Park J. W.., Jung S. A.., Song J. Y.., Choi S. H.., Park S. G.., Choe M. Y.., Lee B. S.., Byun E. Y.., Baik S. C.., Lee W. K.., Cho M. J.., Youn H. S.., Ko G. H.., Rhee K. H.2000. Two-dimensional gel electrophoresis of Helicobacter pylori for proteomic analysis. J. Korean Soc. Microbiol. 35:97–108.
Kim B. W.., Choi M. G.., Choi H.., Moon S. B.., Kim B. K.., Chae H. S.., Kim J. K.., Chung I. S.., Chung K. W.., Sun H. S.., Park D.H.1999. Pooled analysis of antibiotic therapy for Helicobacter pylori eradication in Korea. Korean J. Gastroenterol. 34:42–49.
Kim J. M.2007. Antibiotic resistance in Helicobacter pylori. Hanyang Med. Rev. 27:80–95.
Kim J. M.., Kim J. S.., Jung H. C.., Kim N.., Kim Y. J.., Song I. S.2004. Distribution of antibiotic MICs for Helicobacter pylori strains over a 16-year period in patients from Seoul, South Korea. Antimicrob. Agents Chemother. 48:4843–4847.
Kim S. H.., Kim O. J.2004. Application of consensus polymerase chain reaction for monitoring of Helicobacter species. Lab. Animal. Res. 20:316–320.
Koehn F. E.., Carter G. T.2005. The evolving role of natural products in drug discovery. Nat. Rev. Drug Discov. 4:206–220.
Lee J.., Kim S. M.., Im E. H.., Choi Y. W.., Kim Y. M.., Kim P. S.., Lee J. H.2005. The prevalence of antimicrobial resistance in Helicobacter pylori isolated in Daejeon. Korean J. Clin. Microbiol. 8:47–50.
Lee J. Y.., Kim W.., Gawk G. Y.., Park S. C.., Ye B. D.., Lee S. H.., Kim S. G.., Kim J. S.., Jun H. C.., Song I. S.2002. Reinfection rate and clinical manifestation of Helicobacter pylori-positive peptic ulcer disease after triple therapy containing clarithromycin. Korean J. Gastrornterol. 39:93–100.
Lim T. H.., Lee J. M.., Cha B. J.2002. Antifungal activity and identification of an Actinomycetes straun isolated from mummified peaches. Kor. J. Appl. Microbiol. Biotechnol. 28:161–166.
Marshall B. J.., Warren J. R.1984. Unidentified curved bacilli in the stomach of patients with gastric and peptic ulceration. Lancet. 1:1311–1315.
Nguyen T.T.., Cho S.O.., Ban J.Y.., Kim J.Y.., Ju H.S.., Koh S.B.., Song K.S.., Seong Y.H.2008. Neuroprotective effect of Sanguisorbae radix against oxidative stress-induced brain damage: in vitro and in vivo. Biol. Pharm. Bull. 31(11):2028–2035.
Park H. J.., Kim J. W.., Lee J. H.., Shin J. H.., Yu K. A.2000. Detection of clarithromycin resistant Helicobacter pylori by polymerase chain reaction. Korean J. Gastroenterol. 47:459–461.
Park K.H.., Koh D.., Kim K.., Park J.., Lim Y.2004. Antiallergic activity of a disaccharide isolated from Sanguisorba officinalis. Phytother. Res. 18(8):658–662.
Reher G.., Budesinsky M.1992. Triterpenoids from plants of the anguissorbeae. Phytochemistry. 31:3909–3914.
Shim S. G.., Kim J. J.., Kim Y. H.., Sung I. K.., Son H. J.., Lee K. T.., Rhee P. L.., Koh K. C.., Paik S. W.., Rhee J. C.., Choi K. W.., Kim C. S.., Choi M. S.., Ryu K. H.., Lee, H. Y. Heo J. S.., Noh J.H.2000. One-week triple therapy for Helicobacter pylori a prospective, randomized study. Korean J. Gastroenterol. 35:16–22.
Tanaka T.., Nonaka G.., Nishioka I.1983. 7-O-Galloyl-(+)catechin and 3-O-galloylprocyanidin B-3 from Sanguisorba officinalis. Phytochemistry. 22:2575–2578.
Velazquez M.., Feirtag J. M.1999. Helicobacter pylori: characteristics, pathogenicity, detection methods and mode of transmission implicating foods and water. Int. J. Microbiol. 53:95–104.
53, 95-104. Wouden E.., Thijs J.., Zwet A.., Sluiter W.., Kleibeuker J.1999. The influence of in vitro nitroimidazole resistance on the efficacy of nitroimidazole-containing anti-Helicobacter pylori regimens: a metaanalysis. Am. J. Gastroenterol. 94:1751–1759.
Table 1.
Table 2.
Group | Treatment | Week after inoculation | ||||
---|---|---|---|---|---|---|
0 | 1 | 2 | 3 | 4 | ||
I | H. pylori+Sanguisorbaa | 132.5± 2.0 | 136.0±2.1 | 140.0±2.1∗ | 142.5±1.6∗ | 144.0±1.1∗ |
II | H. pylori+PBS | 132.5±1.5 | 135.0±2.0 | 135.0±2.1 | 135.5±2.0 | 136.5±1.6 |
III | PBS+Sanguisorba | 133.0±2.1 | 138.0±2.1 | 142.0± 2.0∗ | 144.5±2.0∗ | 145.0±2.5∗ |
IV | PBS+PBS | 133.5±2.1 | 138.5±1.1 | 143.0±1.5∗ | 145.0±2.0∗ | 146.0±2.5∗ |
Table 3.
Group | Treatment | Gross lesion scores | Histopathological lesion scores |
---|---|---|---|
I | H. pylori+Sanguisorba | 12.0±3.5∗ | 2.0±0.50∗ |
II | H. pylori+PBS | 95.0±5.5 | 8.0±1.50 |
III | PBS+Sanguisorba | 0∗ | 0∗ |
IV | PBS+PBS | 0∗ | 0∗ |
Table 4.
Group | Inoculationa | n | Positive reaction (positive percent) b | ||
---|---|---|---|---|---|
H. pylori | Treatment | CLO | PCR | ||
I | Yes | Sanguisorba | 10 | 0∗ (0 %, CI c 0-25.9) | 0∗ (0 %, CI 0-25.9) |
II | Yes | PBS | 10 | 10 (100 %, CI 74.1-100) | 10 (100 %, CI 74.1-100) |
III | No | Sanguisorba | 10 | 0∗ (0 %, CI 0-25.9) | 0∗ (0 %, CI 0-25.9) |
IV | No | PBS | 10 | 0∗ (0 %, CI 0-25.9) | 0∗ (0 %, CI 0-25.9) |