Hydrogen Protects Mitochondrial Function by Increasing the Expression of PGC-1α and Ameliorating Myocardial Ischaemia-Reperfusion Injury.
Yue Zuo, Jiawei Wang, Zhexuan Gong, Yulong Wang, Qiang Wang, Xueyang Yang, Fulin Liu, Tongtong Liu · Journal of cellular and molecular medicine · 2024
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H2HUBB TAKEAWAY
In a laboratory model, the mortality rate of H9C2 cardiomyocytes was observed using the TUNEL assay, and as shown in the images (Figure 2G,H ), the cell mortality rate was greater than 80% after HR injury and significantly lower (less than 30%) after H₂ treatment. The authors concluded that 5 The main conclusions of this study are as follows. The application of H₂ can reduce myocardial I/R injury, the deletion of PGC‐1α weakened the protective effect of H₂ on I/R heart, H₂ ameliorates myocardial cell inflammatory response and oxidative stress under HR injury by acting on PGC‐1α, H₂ can exert mitochondrial protection function and this effect is absolved by PGC‐1α deletion under the condition of HR injury. These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
What the Findings Mean
H2HUBB reviewed how molecular hydrogen was evaluated in this publication and summarizes the source-grounded findings below. The mortality rate of H9C2 cardiomyocytes was observed using the TUNEL assay, and as shown in the images (Figure 2G,H ), the cell mortality rate was greater than 80% after HR injury and significantly lower (less than 30%) after H₂ treatment.
What the Researchers Studied
The study used a in vitro cell-culture laboratory experiment. The comparison condition was control condition or baseline measurements.
What Effects Did Molecular Hydrogen Have?
Saturated hydrogen‐rich water KHB with 1 g of hydrogen‐rich powder was added to every 100 mL of KHB [the hydrogen‐rich powder was provided by Li Zhilin, a teacher from Hebei University]. The hearts were randomly divided into three groups ( n = 10): (A) the control group (sham), which was perfused with KHB for 50 min. (B) the ischaemia/reperfusion group (I/R), which was perfused with KHB for 10 min, followed by total myocardial ischaemia for 20 min and reperfusion of KHB for 20 min; and (C) the hydrogen‐rich water I/R group (I/R + H₂ ), which was perfused with KHB for 10 min, total myocardial ischaemia for 20 min and saturated hydrogen‐rich water for reperfusion of KHB for 20 min. PGC‐1α gene knockdown group (SiRNA): H9C2 cells were transiently transfected for PGC‐1α gene knockdown followed by normal cell culture. C. cell hypoxia/reoxygenation group (HR): normally cultured H9C2 cells were subjected to hypoxia and then reoxygenated with reoxygenation solution; D. cell hypoxia/reoxygenation group under the intervention of hydrogen‐rich water (HR + H₂ ): cells were treated as in group C and subjected to a reoxygenation process of hypoxic/saturated hydrogen‐rich water reoxygenation solution for normally cultured H9C2 cells; E. hypoxia/reoxygenation group under hydrogen‐rich water intervention after PGC‐1α gene knockdown (HR + H₂ + SiRNA): H9C2 cells transiently transfected for PGC‐1α gene knockdown were treated as in group C and subjected to a reoxygenation process of hypoxia/saturated hydrogen‐rich water reoxygenation solution. The mortality rate of H9C2 cardiomyocytes was observed using the TUNEL assay, and as shown in the images (Figure 2G,H ), the cell mortality rate was greater than 80% after HR injury and significantly lower (less than 30%) after H₂ treatment. The authors concluded that 5 The main conclusions of this study are as follows. The application of H₂ can reduce myocardial I/R injury, the deletion of PGC‐1α weakened the protective effect of H₂ on I/R heart, H₂ ameliorates myocardial cell inflammatory response and oxidative stress under HR injury by acting on PGC‐1α, H₂ can exert mitochondrial protection function and this effect is absolved by PGC‐1α deletion under the condition of HR injury. Western blot analysis revealed that H/R damage significantly increased the PGC‐1α expression in H9C2 cells compared to that in the control group, and H₂ further enhanced this alteration, suggesting that hydrogen‐rich water promotes HR‐mediated PGC‐1α upregulation (Figure 2B,C ).
Why These Findings Matter
These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
How Strong Is This Evidence?
This is laboratory evidence from a in vitro cell-culture laboratory experiment. It is most informative for the biological mechanisms, cellular responses, or biochemical outcomes directly measured.
Technical Study Details
H2HUBB classifies this publication as laboratory study with laboratory or cellular evidence. The reported sample size was 1. The study used a in vitro cell-culture laboratory experiment.
Limitations and Safety
No separate limitations or safety findings were identified in the current-study source text available to H2HUBB.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base.