General Research
Model: human
Hydrogen-rich medium ameliorates lipopolysaccharides-induced mitochondrial fission and dysfunction in human umbilical vein endothelial cells (HUVECs) via up-regulating HO-1 expression
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How Hydrogen Therapy May Help Protect Against Inflammation and Cellular Damage
A recent study found that hydrogen-rich medium can help protect human cells from damage caused by toxins. The study's findings suggest that hydrogen therapy may have a role to play in protecting us against diseases and conditions like sepsis, chronic fatigue syndrome, and lung disease. With its potential to reduce inflammation and oxidative stress, hydrogen therapy is an exciting area of research that could have significant implications for our overall health.
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Publish Year 2022 Country China Rank Positive Journal International Immunopharmacology Primary Topic Whole Body Secondary TopicSepsis Model Cell Culture Tertiary TopicMitochondrial Function Vehicle Medium (Dissolved) pH Neutral Application Culture Media Comparison Complement
Background
Methods: HUVECs cells cultured with medium which contained Lipopolysaccharides (LPS), Saline, hydrogen, Mdivi-1 (a dynamin-related protein 1 [Drp1] inhibitor) or zinc protoporphyrin IX (Znpp) (a HO-1 inhibitor) were also used in the research. Cell death and apoptosis were assessed using FITC annexin V and PI. Mitochondria were stained with Mitotracker orange and observed by confocal microscope. Oxygen consumption rate was assessed by seahorse xf24 extracellular analyzer. Mitochondrial membrane potential monitored by JC-1 dye. The expressions of Drp1 and HO-1 were tested by Western blot. The co-localization of Drp1 and mitochondria was determined by immunofluorescence.
Methods
Results: LPS caused a decrease in ATP content, mitochondrial membrane potential, and maximal respiration rate. At the same time, increased expression of Drp1 were observed in LPS-stimulated HUVECs, concomitantly with excessive mitochondrial fission. We found that hydrogen-rich medium can increase ATP content, mitochondrial membrane potential and maximal respiration rate, and decrease the expression of Drp1 in LPS-treated HUVECs. Meanwhile, hydrogen can ameliorate excessive mitochondrial fission caused by LPS. Furthermore, hydrogen-rich medium had a similar effect to Mdivi-1, a mitochondrial fission blocker. Both of them rescued the up-regulation of Drp1 and mitochondrial fission induced by LPS, then normalized mitochondrial shape after LPS stimulation. But after Znpp pretreatment, HO-1 expression was inhibited and the protective effects of hydrogen were abrogated. Conclusions: Hydrogen-rich medium can alleviate the LPS-induced mitochondrial fusion/fission and dysfunction in HUVECs via HO-1 up-regulation.