Abstract
Helicobacter pylori, a pathogen responsible for gastric and duodenal diseases, absorbs various steroid compounds into the cell membrane even though some are toxic to this bacterium. An earlier study by our group has demonstrated that progesterone is bactericidal to H. pylori. In this study, we newly synthesized a steroid compound, 17α-hydroxyprogesterone linoleic acid ester (17hPL), to examine antibacterial activity against H. pylori. As expected, 17hPL acted as a bactericidal agent to H. pylori and had no effect on the survival of other common bacterial species. This steroidal substance interacted with phosphatidylethanolamine (PE) on the outer membrane of H. pylori to induce the release of PE from the bacterial cell membrane and to ultimately lyse the bacterial cells. One of the hormonal effects of progesterone is the inhibition of nitric oxide (NO) production from mouse macrophages activated by lipopolysaccharide (LPS). We therefore examined the inhibition effect of 17hPL on the NO production of RAW 264.7 cells, a murine macrophage-like cell line, stimulated with LPS and demonstrated that 17hPL is relatively weaker in its capability to inhibit NO production in LPS-activated cells than progesterone. These results suggest the possibility that 17hPL could be an oral medicine for selectively treating patients infected with H. pylori.
| Original language | English |
|---|---|
| Pages (from-to) | 17-25 |
| Number of pages | 9 |
| Journal | Journal of Steroid Biochemistry and Molecular Biology |
| Volume | 140 |
| DOIs | |
| Publication status | Published - 2014 |
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Keywords
- 17α- Hydroxyprogesterone
- 17α-Hydroxyprogesterone caproate
- 17α-Hydroxyprogesterone linoleic acid ester
- 2,6-di-O-methyl-β-cyclodextrin
- Helicobacter pylori
- Progesterone
ASJC Scopus subject areas
- Biochemistry
- Clinical Biochemistry
- Endocrinology
- Cell Biology
- Molecular Biology
- Endocrinology, Diabetes and Metabolism
- Molecular Medicine
Cite this
Antibacterial activity of a novel synthetic progesterone species carrying a linoleic acid molecule against Helicobacter pylori and the hormonal effect of its steroid on a murine macrophage-like cell line. / Amgalanbaatar, Avarzed; Shimomura, Hirofumi; Hosoda, Kouichi; Hayashi, Shunji; Yokota, Kenji; Hirai, Yoshikazu.
In: Journal of Steroid Biochemistry and Molecular Biology, Vol. 140, 2014, p. 17-25.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Antibacterial activity of a novel synthetic progesterone species carrying a linoleic acid molecule against Helicobacter pylori and the hormonal effect of its steroid on a murine macrophage-like cell line
AU - Amgalanbaatar, Avarzed
AU - Shimomura, Hirofumi
AU - Hosoda, Kouichi
AU - Hayashi, Shunji
AU - Yokota, Kenji
AU - Hirai, Yoshikazu
PY - 2014
Y1 - 2014
N2 - Helicobacter pylori, a pathogen responsible for gastric and duodenal diseases, absorbs various steroid compounds into the cell membrane even though some are toxic to this bacterium. An earlier study by our group has demonstrated that progesterone is bactericidal to H. pylori. In this study, we newly synthesized a steroid compound, 17α-hydroxyprogesterone linoleic acid ester (17hPL), to examine antibacterial activity against H. pylori. As expected, 17hPL acted as a bactericidal agent to H. pylori and had no effect on the survival of other common bacterial species. This steroidal substance interacted with phosphatidylethanolamine (PE) on the outer membrane of H. pylori to induce the release of PE from the bacterial cell membrane and to ultimately lyse the bacterial cells. One of the hormonal effects of progesterone is the inhibition of nitric oxide (NO) production from mouse macrophages activated by lipopolysaccharide (LPS). We therefore examined the inhibition effect of 17hPL on the NO production of RAW 264.7 cells, a murine macrophage-like cell line, stimulated with LPS and demonstrated that 17hPL is relatively weaker in its capability to inhibit NO production in LPS-activated cells than progesterone. These results suggest the possibility that 17hPL could be an oral medicine for selectively treating patients infected with H. pylori.
AB - Helicobacter pylori, a pathogen responsible for gastric and duodenal diseases, absorbs various steroid compounds into the cell membrane even though some are toxic to this bacterium. An earlier study by our group has demonstrated that progesterone is bactericidal to H. pylori. In this study, we newly synthesized a steroid compound, 17α-hydroxyprogesterone linoleic acid ester (17hPL), to examine antibacterial activity against H. pylori. As expected, 17hPL acted as a bactericidal agent to H. pylori and had no effect on the survival of other common bacterial species. This steroidal substance interacted with phosphatidylethanolamine (PE) on the outer membrane of H. pylori to induce the release of PE from the bacterial cell membrane and to ultimately lyse the bacterial cells. One of the hormonal effects of progesterone is the inhibition of nitric oxide (NO) production from mouse macrophages activated by lipopolysaccharide (LPS). We therefore examined the inhibition effect of 17hPL on the NO production of RAW 264.7 cells, a murine macrophage-like cell line, stimulated with LPS and demonstrated that 17hPL is relatively weaker in its capability to inhibit NO production in LPS-activated cells than progesterone. These results suggest the possibility that 17hPL could be an oral medicine for selectively treating patients infected with H. pylori.
KW - 17α- Hydroxyprogesterone
KW - 17α-Hydroxyprogesterone caproate
KW - 17α-Hydroxyprogesterone linoleic acid ester
KW - 2,6-di-O-methyl-β-cyclodextrin
KW - Helicobacter pylori
KW - Progesterone
UR - http://www.scopus.com/inward/record.url?scp=84889808616&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84889808616&partnerID=8YFLogxK
U2 - 10.1016/j.jsbmb.2013.10.023
DO - 10.1016/j.jsbmb.2013.10.023
M3 - Article
C2 - 24189541
AN - SCOPUS:84889808616
VL - 140
SP - 17
EP - 25
JO - Journal of Steroid Biochemistry and Molecular Biology
JF - Journal of Steroid Biochemistry and Molecular Biology
SN - 0960-0760
ER -