Hydrogen Protects Blood Vessel Cells from Sepsis-Related Damage
- Authors
- Naqi Lian, Xing Mao, Yanchao Su, Yanyan Wang, Yaoqi Wang, Yuzun Wang, Hongguang Chen, Ruqing Zhu, Yonghao Yu, Keliang Xie
- Journal
- International Immunopharmacology
- Year
- 2022
- DOI
- 10.1016/j.intimp.2022.108936
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis
- Body System
- Cardiovascular
TL;DR
Hydrogen treatment helps protect blood vessel cells from damage caused by toxins associated with sepsis by maintaining healthy mitochondrial function.
Key Finding
Hydrogen-rich medium protected human blood vessel cells from bacterial toxin damage by preventing excessive mitochondrial fragmentation and restoring the cells' ability to produce energy, with these effects dependent on activation of a protective protein called HO-1.
Summary
This laboratory study examined how hydrogen-rich water affects human blood vessel cells exposed to lipopolysaccharide (LPS), a bacterial toxin that triggers sepsis (a life-threatening infection response). Researchers found that hydrogen-rich medium helped restore the cells' energy production and prevented abnormal changes in mitochondria (the cell's power plants), and this protection appeared to work through a protein called HO-1.
Practical Takeaway
While this cell-culture study suggests hydrogen may help protect blood vessel cells from sepsis-related damage, it is very early-stage research conducted in laboratory conditions only—not in animals or humans. Much more research would be needed before any conclusions about hydrogen water's usefulness in sepsis or related conditions could be drawn.
Abstract
Background: Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. It has been showed that the change of mitochondrial dynamics has been proved to be one of the main causes of death in patients with severe sepsis. And hydrogen has been proved to exert its protective effects against sepsis via heme oxygenase-1 (HO-1). This study was designed to demonstrate that whether the benefit effects of hydrogen can maintain the dynamic process of mitochondrial fusion/fission to mitigate human umbilical vein endothelial cells (HUVECs) injury exposed to endotoxin through HO-1. 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. 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.