Table 1.

Selected pharmacological and non-pharmacological interventions and their effects on HNE production/utilization in gastric mucosa.

Intervention	Target Process/Pharmacological Effect	References
Proton pump inhibitors, H2 histamine receptor inhibitors	Reduction of acidity, decreased proteolytic activity of gastric juice/decreased gastric injury (production of HNE)	[61,66]
Antibiotics	H. pylori eradication/decreased gastric injury (production of HNE)	[61,66]
NO, CO, H2S-releasing NSAIDs	Release of CO, NO, and/or H2S modulates redox signaling, improves endothelial function, and improves microcirculation/reduced production and improved utilization of HNE	[75,76]
Antioxidants/polyphenols present in food	Reduced lipid peroxidation of PUFAs in stomach/reduced absorption of exogenous HNE	[2,79]
Phytochemical and phytotoxins with moderate prooxidant action	Nrf-2 activators induce expression of antioxidant genes and increase detoxification of HNE	[20,80]
Interval hypoxic training	Improvement of autonomic control of microcirculation and function of internal organs	[81,82]
Exercise, intermittent fasting, caloric restriction	Activation of autophagy, reduction of systemic inflammatory response, improvement of protein quality control and autonomic regulation	[83]
Ulcer-healing drugs (actovegin, solcoseryl etc.)	Mechanism unknown, suggested influence on microcirculation and/or endothelial function	[84,85]