Hemin protects against CFS-like symptoms in mice

Porphyria therapy may have potential as a treatment in ME/CFS

Derived from red blood cells, hemin is a drug sometimes used to treat the symptoms of porphyria, such as pain and increased heart rate. Researchers from India wondered whether hemin might be of some benefit in ME/CFS, and recently published the results of a study looking at its effects in mice with CFS-like symptoms.

Read the abstract by Thakur and colleagues in Neurotoxicity Research

Key findings

  • A CFS-like condition was induced in experimental mice, resulting in decreased activity, increased immobility and raised anxiety levels.
  • Treatment with hemin for 21 days improved all these symptoms, and also reduced oxidative stress, mitochondrial dysfunction and changes in the levels of several neurotransmitters.
  • It remains to be seen whether hemin has any effect in humans with ME/CFS, and might therefore be used as a therapy to alleviate symptoms.

What did they do?

The researchers induced a CFS-like condition in the mice using a forced-swimming test, a technique in which mice are placed into water and forced to swim and float for a short period of time each day. The condition is characterised by a significant decrease in activity, an increase in immobility and an increase in an anxiety-like state.

Some mice with induced CFS were then treated daily with hemin (at one of two doses) for 21 days, while another group was left untreated, and a third group comprised healthy mice. Various behavioural measures (immobility period, locomotor activity, grip strength and anxiety levels) were assessed throughout the study period.

What did they find?

By day 21, treatment with hemin had resulted in significant improvements in all of the parameters measured, including immobility time, locomotor activity, grip strength and anxiety-like behaviour. 

The brains of mice in all three treatment groups were analysed at the end of the study period. Compared with the healthy mice, those with induced CFS-like symptoms had an increase in oxidative stress and mitochondrial dysfunction, and changes in the levels of several neurotransmitters (catecholamines) and their metabolites. However, these measures were reduced in mice that had been treated with hemin.

Hemin induces the enzyme Heme oxygenase 1 (HO-1), which is known to protect against oxidative stress and performs a critical role in the prevention of vascular inflammation. When HO-1 was inhibited, the benefits of hemin treatment were reduced, showing that this enzyme is essential in the protective effects of hemin.

What does this mean?

The addition of hemin provided some protection against the symptoms of an induced CFS-like condition in mice.

Hemin is currently used to control the symptoms of porphyria (such as pain and increased heart rate), but it is only administered under very strict conditions as it can cause side effects, especially in the kidneys.

This study was carried out in mice, so it is not yet clear whether hemin might be an effective treatment to alleviate symptoms in people with ME/CFS, or have any impact on long-term, established illness. However, this is certainly an area we will be watching with interest.

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