More and more evidence suggests that neuroinflammation characterized by immune cell infiltration, mast cell and glial cell activation, and the production of inflammatory mediators in the peripheral and central nervous system plays an important role in the induction and maintenance of chronic inflammation. Palmitoylethanolamide is a N-acylethanolamide and a lipid with anti-inflammatory effects. However, very little is known about its analgesic effect in chronic pain.
Palmitoylethanolamide bulk powder is an endogenous fatty acid amide with a chemical structure of N-(2-hydroxyethyl)esadecanamides and is considered to be a self-substance. Specifically, it is mainly known as an anti-inflammatory agent due to downregulation of mediators released by mast cells, monocytes, and macrophages. Recently, it has been shown that palmitoylethanolamide has a powerful ability to modulate complex systems involving inflammation, pruritus, neuropathic, and nociceptive pain.
Palmitoylethanolamide is generally considered to be involved in endogenous defense mechanisms triggered by various forms of tissue damage or endogenous inflammation and nociceptive fiber stimulation. It consists of N-acylethanolamide and lipids and is known to have anti-inflammatory effects. Unlike its anti-inflammatory effects, its analgesic effect in chronic pain is little known. Numerous studies have shown that palmitoylethanolamide can alleviate the degree of pain with no harmful side effects in humans. In animal experiments, palmitoylethanolamide may have anti-inflammatory and analgesic effects in certain conditions related to inflammation and pain.
Palmitoylethanolamide has broad analgesic effects and these effects have been tested in many different types of pain models. It alleviates pain behavior induced by formalin, magnesium sulfate, carrageenan, nerve growth factor, and turpentine oil. In addition, palmitoylethanolamide has been reported to inhibit pain hypersensitivity following sciatic nerve ligation in a neuropathic pain model. Palmitoylethanolamide may be involved in endogenous regulation of nociception because its analgesic effect occurs rapidly and before its anti-inflammatory effect. However, the specific analgesic mechanism of palmitoylethanolamide is currently unclear.
When monoiodoacetic acid (MIA) is locally injected into the joint, it rapidly induces inflammation, interrupts the metabolism of chondrocytes, and then induces cartilage degeneration. In addition, MIA-induced rat osteoarthritis is similar to human osteoarthritis in terms of cartilage and skeletal pathological features and can be used as a minimally invasive animal model.
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