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Linolenic acid-metronidazole inhibits the growth of Helicobacter pylori through oxidation
Wen-Ting Zhou1, Yuan-Yuan Dai2, Li-Juan Liao1
1School of Basic Medicine, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China.
Background:
Resistance to antibiotics is one the main factors constraining the treatment and control of Helicobacter pylori (H. pylori) infections. Therefore, there is an urgent need to develop new antimicrobial agents to replace antibiotics. Our previous study found that linolenic acid-metronidazole (Lla-Met) has a good antibacterial effect against H. pylori, both antibiotic-resistant and sensitive H. pylori. Also, H. pylori does not develop resistance to Lla-Met. Therefore, it could be used for preparing broad-spectrum antibacterial agents. However, since the antibacterial mechanism of Lla-Met is not well understood, we explored this phenomenon in the present study.
Aim:
To understand the antimicrobial effect of Lla-Met and how this could be applied in treating corresponding infections.
Methods:
H. pylori cells were treated with the Lla-Met compound, and the effect of the compound on the cell morphology, cell membrane permeability, and oxidation of the bacteria cell was assessed. Meanwhile, the differently expressed genes in H. pylori in response to Lla-Met treatment were identified.
Results:
Lla-Met treatment induced several changes in H. pylori cells, including roughening and swelling. In vivo experiments revealed that Lla-Met induced oxidation, DNA fragmentation, and phosphatidylserine ectropionation in H. pylori cells. Inhibiting Lla-Met with L-cysteine abrogated the above phenomena. Transcriptome analysis revealed that Lla-Met treatment up-regulated the expression of superoxide dismutase SodB and MdaB genes, both anti-oxidation-related genes.
Conclusion:
Lla-Met kills H. pylori mainly by inducing oxidative stress, DNA damage, phosphatidylserine ectropionation, and changes on cell morphology.
Insights
Linolenic acid-metronidazole (Lla-Met) effectively combats Helicobacter pylori by inducing oxidative stress and DNA damage. This novel compound shows promise as a broad-spectrum antibacterial agent against H. pylori infections.
Area of Science:
- Microbiology
- Drug Discovery
- Antimicrobial Resistance
Background:
- Antibiotic resistance in *Helicobacter pylori* (*H. pylori*) poses a significant challenge for infection treatment.
- New antimicrobial agents are urgently needed to overcome resistance and treat *H. pylori* infections.
- Linolenic acid-metronidazole (Lla-Met) demonstrates broad-spectrum antibacterial activity against *H. pylori* without inducing resistance.
Purpose of the Study:
- To elucidate the antimicrobial mechanism of Lla-Met against *H. pylori*.
- To investigate the effects of Lla-Met on *H. pylori* cell morphology, membrane permeability, and oxidation.
- To identify gene expression changes in response to Lla-Met treatment.
Main Methods:
- Treatment of *H. pylori* cells with Lla-Met.
- Assessment of cell morphology, membrane permeability, and oxidation.
- Transcriptome analysis to identify differentially expressed genes.
Main Results:
- Lla-Met induced significant changes in *H. pylori* cell morphology, including roughening and swelling.
- Lla-Met treatment led to oxidation, DNA fragmentation, and phosphatidylserine ectropionation in *H. pylori* cells.
- Upregulation of anti-oxidation genes (*SodB*, *MdaB*) was observed following Lla-Met treatment.
Conclusions:
- Lla-Met effectively kills *H. pylori* by inducing oxidative stress and DNA damage.
- Morphological changes and phosphatidylserine ectropionation are key mechanisms of Lla-Met's action.
- Lla-Met represents a promising therapeutic agent for *H. pylori* infections.
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