Selenium Reduced Pain in Fibromyalgia Rat Model, Study Reports

Selenium Reduced Pain in Fibromyalgia Rat Model, Study Reports

A recent study in rats describes a new mechanism that is responsible for mediating pain in fibromyalgia (FM), providing a potential new avenue to alleviate pain symptoms in this patient population.

The study, “Involvement of TRPM2 and TRPV1 channels on hyperalgesia, apoptosis and oxidative stress in rat fibromyalgia model: Protective role of selenium,” was published in the journal Scientific Reports.

Previous studies suggest that the pain associated with FM is characterized by low levels of the mineral selenium, as well as excessive calcium influx, reactive oxygen species (ROS) production, and acidic pH.

Two acid- and oxidative stress-sensitive channels belong to the transient receptor potential (TRP) family: TRPM2 and TRPV1. These are calcium cation channels that, when stimulated, allow the influx of calcium into the cell.

These channels are mainly expressed in the dorsal root ganglion neural (DRGN) cells and the sciatic nerve neural (SciN) cells. These two cell types are importation for the induction of pain in FM.

Researchers used a rat model to better understand the role of the TRPM2 and TRPV1 channels in oxidative stress and acid-dependent activation of pain in FM, and the therapeutic potential of selenium.

Because FM is more common in women, the researchers used female rats. They divided 36 rats into four treatment groups: control, selenium-treated, FM rats, and FM rats treated with selenium.

When selenium was given to FM rats, there was a significant reduction in pain sensitivity in the animals. Additionally, treating rats with selenium before inducing FM could increase the sensitivity threshold, allowing the animals to endure higher levels of mechanical pain stimuli.

The researchers also showed that blocking the TRPV1 and TRPM2 channels with specific inhibitors could effectively reduce the intracellular concentration of calcium in DRGN and SciN cells.

Importantly, this effect on calcium levels could also be seen when selenium was given to rats. This suggests that selenium can regulate FM-induced calcium influx by regulating the TRPV1 and TRPM2 calcium channels in neurons.

Similarly, when stimulated by oxidative stress, an increase in calcium concentration was observed, but this effect could be minimized by treatment with selenium.

When DGRN and SciN are stimulated by ROS or other means, often these cells undergo a type of programmed cell death called apoptosis. An increase in apoptotic markers and decrease in cell viability was seen in FM-induced rats. Importantly, treatment with selenium lessened this effect and increased cell viability.

This model, therefore, provides a new understanding of the underlying causes of FM-associated pain, as well as new potential therapeutic avenues.

“The use of Se [selenium] may be an effective novel approach for treating FM-induced pain, mitochondrial oxidative stress, and apoptosis. In addition, the TRPM2 and TRPV1 channels may be important pharmacological targets in the treatment of FM-induced apoptosis and pain,” the team concluded.


  1. Denise Bault says:

    I’m curious. How do you give a female rat fibromyalgia? And if you know HOW to give one fibromyalgia, wouldn’t you know the cause and therefore the cure?

    • Cindy says:

      Very good points Denise. Indeed how does a researcher give a female rat fibromyalgia. Stress them out to the max or what? You would think that knowing the cause would lead to a cure. I wondered this myself when I read the story.

    • Mickey Nice says:

      I was thinking the same thing. How do you know a rat has fibromyalgia. And how do you know what the pain levels are. Mr. Rat, are you at a 10 level pain today or a 3.

    • Sean says:

      It’s a model for fibromyalgia, “induced hyperalgesia”, not fibromyalgia itself.

      From the study itself:
      “Induction of hyperalgesia
      For produce a bilateral long-lasting hyperalgesia similar to fibromyalgia in humans, acidic saline solution (adjusted to pH 4.0) was injected into the gastrocnemius muscle in the rats4. Before the first injection of acidic or normal saline into the gastrocnemius muscle, paw withdrawal threshold values of the rats were recorded in order to record the baseline value. Each animal received two repeated injections of the acidic saline solution (100 μl) in the same unilateral gastrocnemius muscle under propofol inhaled anesthesia, a procedure which is repeated five days later4. After the second injection of the acidic saline, hyperalgesia in the animal is detected increase the paw withdrawal threshold by the von Frey filament and hot plate tests in the muscle.”

  2. Will Shirley says:

    I’d like to know why sudden changes in weather can cause flares of pain at odd spots on the body. How does a mineral deficiency work there? Speaking as a fibro sufferer who lives in the NE, winter pain sucks and I take every mineral linked to the pain without much impact…

  3. Sandra VanHouten says:

    I read a study by a Dr. Rice who found an excessive number of AV shunts in the hands of Fibro patients (also found in feet). Dr. Rice found that these shunts which are to regulated blood flow also have nerve ending. He believes these excessive number of shunts are disrupting normal blood flow. Thus not getting oxygen and other nutrients into the deep muscles or brain. Also I read a study from NHI (National Health Institute) that many fibro symptoms are similar to vitamin B6 deficiency. Also read fibro patients have low vitamin D and low magnesium levels. I don’t understand why someone is not tracking or combining all this research data to find a cause and cure. Dr. Rice’s finding of the excessive AV shunts were published in June 2013. Almost 5 years ago!

  4. Najla says:

    I have read a LOT of studies about how mineral deficiencies can cause some of the fibromyalgia symptoms . What I would like to know more is why even if vitamin/mineral replacement, fibro patients continue to experience those symptoms.
    We need to be aware that vitamins and minerals in excess can be as dangerous as the lack of them. And that they also can interact with our meds. Talk to your doctor before increasing your vitamin intake.

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