Paper 5

Far Infrared Irradiation Restores Mitochondrial Dynamics and Function, Significantly Reducing Brain Injury

Abstract

This study applied a far infrared (FIR) irradiation protocol using the patented EEFIT LITE® device, which emits a precisely defined spectrum within the 4–20 μm range,a bandwidth known for its specific biological effects. The core technical parameter of this device is its accurate spectral output. The aim of this research was to systematically evaluate its effectiveness in restoring mitochondrial balance and function.

Objective
Ischemic stroke occurs when a blood vessel in the brain becomes blocked, depriving brain cells of oxygen and leading to damage or death. It is one of the leading causes of adult disability and mortality worldwide. Existing treatments often carry side effects, such as an increased risk of bleeding. Therefore, there is an urgent need to develop safe, non-pharmacological, and non-invasive therapeutic approaches. This study investigated whether FIR irradiation can reduce stroke-induced brain injury and explored the underlying protective mechanisms.

Methods
The research team used a rat model of middle cerebral artery occlusion to simulate the brain damage caused by ischemic stroke in humans. The rats were divided into four groups: a healthy control group, an untreated stroke group, a stroke group that received daily 30-minute FIR irradiation for 14 days, and a stroke group treated with standard medication. In parallel, the team cultured nerve cells in the laboratory and subjected them to oxygen deprivation to mimic stroke-related cellular damage, in order to verify the effects of FIR on injured cells. The groups were then compared in terms of motor function, extent of brain damage, survival rates, and detailed analyses of brain tissue changes and protective mechanisms.

Key Findings

1. Reduction in brain damage severity after stroke
In stroke-induced rats that received FIR irradiation, cerebral infarct volume was significantly reduced by approximately 40% in the early stages (days 1 and 3) compared to the untreated group. Brain edema and neurological deficits were also markedly improved.

Rats that received FIR irradiation showed an approximately 40% reduction in brain damage, indicating that FIR therapy can significantly improve stroke-induced brain injury.

2. Consistent reduction in infarct volume and significant improvement in neurological scores
FIR irradiation steadily reduced infarct volume and significantly lowered neurological deficit scores at all time points measured during the experimental period.

FIR-irradiated rats exhibited significantly reduced neurological deficit scores.

3. Significant improvements in brain edema, body weight, survival rate, and relative cerebral blood flow
Following FIR irradiation, brain edema was notably alleviated, body weight remained stable, the 14‑day survival rate increased from 25% to 60%, and relative cerebral blood flow showed partial recovery, indicating improved blood supply to the brain.

The survival rate of FIR-treated rats increased from 25% to 60%.

4. Effects comparable to the standard stroke drug nimodipine, without side effects
In terms of improving neurological deficits and reducing cerebral infarct volume, FIR irradiation demonstrated protective effects similar to those of the stroke medication nimodipine. Importantly, no side effects—such as the weight loss commonly observed with the drug—were noted during the treatment period.

The effect of FIR irradiation on reducing cerebral blood flow impairment was comparable to that of the stroke drug nimodipine.

5. Regulation of mitochondrial dynamics and energy production
In an in vitro cell model, FIR irradiation significantly restored ATP production in cells damaged by oxygen‑glucose deprivation (an increase of approximately 330 pmol/10⁶ cells). Further animal studies confirmed that FIR effectively restored normal mitochondrial morphology and function, thereby promoting cellular energy metabolism.

In an in vitro cell model, FIR irradiation significantly restored ATP production in damaged cells. Further animal experiments confirmed that FIR helps restore normal mitochondrial morphology and function, thereby promoting cellular energy metabolism.

6. Reduction of oxidative stress and inflammation
FIR irradiation alleviated ischemia‑induced oxidative stress and suppressed the production of inflammatory factors, helping to reduce secondary damage to the brain following stroke. Specifically, 4‑HNE levels in FIR‑treated rats decreased by 2.9 μg/mL, indicating a reduction in oxidative stress and inflammation.

In FIR-treated rats, 4-HNE levels decreased by 2.9 μg/mL, indicating that FIR alleviates ischemia-induced oxidative stress and suppresses the production of inflammatory factors.

Conclusion
This study demonstrates that FIR irradiation within a specific spectral band can restore mitochondrial dynamics and function through physical intervention, significantly reducing brain damage following ischemic stroke. These findings provide important preclinical evidence for the development of safe, non-invasive therapeutic strategies for stroke treatment.

Extended Reading: Mitochondrial Function - International Consensus

Multiple studies have highlighted the central role of mitochondria in maintaining overall health. Key perspectives from related research include:

Core role in energy supply: Mitochondria continuously produce ATP to fuel all physiological activities, and their normal function is fundamental to sustaining life and health (Nature Cell Biology, 2018).
Maintenance of homeostasis under stress: Proteins such as Opa1 within mitochondria help preserve their structural integrity, enabling them to maintain energy production even under metabolic stress (e.g., hypoxia) and preventing energy depletion (Li et al., 2022b).
A line of defense for cell survival: Properly functioning mitochondria not only provide stable energy supply but also protect cells from unnecessary loss by regulating membrane potential and cell death pathways, thereby ensuring normal tissue function (Bonora et al., 2022; Mendoza et al., 2024).

References

Focusing on mitochondrial form and function. Nat Cell Biol. 2018 Jul;20(7):735. (Published in a leading journal in the field of cell biology)
Bonora M, Giorgi C, Pinton P (2022) Molecular mechanisms and consequences of mitochondrial permeability transition. Nat Rev Mol Cell Biol 23:266-285. (Published in the highest-impact review journal in molecular cell biology)
Mendoza A, Patel P, Robichaux D, Ramirez D, Karch J (2024) Inhibition of the mPTP and lipid peroxidation is additively protective against I/R injury. Circ Res 134:1292-1305. (Published in a top-tier journal in cardiovascular research)
Li X, Li H, Xu Z, Ma C, Wang T, You W, Yu Z, Shen H, Chen G (2022b) Ischemia-induced cleavage of OPA1 at S1 site aggravates mitochondrial fragmentation and reperfusion injury in neurons. Cell Death Dis 13:321. (Published in a leading journal in the field of cell death, under Nature Publishing Group)