Neuro-Protective Properties of Progesterone Injection


Neuro-Protective Properties of Progesterone Injection

Diabetes mellitus can lead to several complications especially diabetic neuropathy, nephropathy and retinopathy which can lead to sensory/motor loss, renal failure and blindness, respectively1. The earliest complication observed is diabetic poly-neuropathy was that it affects peripheral, sensory, motor and autonomic nerves2.

Consequent to neurological complications, diabetic patient often complain of wounds or wound deterioration due to sensory nerve affection or falls accompanied by fractures due to motor nerve function deterioration3. Therefore, protection of diabetic patients against poly-neuropathy is vital to avoid further complications. Myelinated nerve fibers have 10 times nerve conduction velocity than the un-myelinated nerve fibers4.

Schwann cells has a major role in peripheral nerve myelination as these cells produce myelin-associated proteins such as myelin-associated glycoprotein (MAG), myelin basic protein (MBP) and myelin protein zero5. A new study was carried out to study the morphometric changes after progesterone administration in the diabetic peripheral nerves and evaluate the protecting effects of progesterone against the degenerative changes of diabetes6.

It was showed that the diameters of the myelinated nerve fibers and axons were significantly decreased in the diabetic nerves. Progesterone administration showed significant increase in the diameter of the myelinated nerve fibers in the diabetic nerves. The exact mechanism of such improvement is not very clear, however, it was postulated that it reduces myelin infolding.

The diameter of the myelinated nerve fibers was significantly increased after administration of the progesterone. This could be probably due to the significant increase in the myelin thickness shown in the current study. Such an increase could be due to stimulation of the expression of myelin proteins by progesterone.

Major effects of progesterone on neurons and glial cells are mediated by its metabolite allopregnanolone which is a potent positive modulator of g-aminobutyric acid type A (GABAA) receptors. Recently, the antagonism of sigma-1 (s1) receptors by progesterone has been shown to be involved in acute neuroprotection after ischemic brain damage7.

It can be concluded that progesterone has a neuroprotective effects on the diabetic nerves. It corrects the loss, number, diameters, surface areas and myelin sheaths of myelinated nerve fibers. It deserves more clinical trials.


Diabetes, progesterone, myelinated nerve fibers, myelin sheath, peripheral nerves,neuroprotective effects, myelin sheaths, myelinated nerve.


  1. Fowler, M.J., 2008. Microvascular and macrovascular complications of diabetes. Diabetes, 26: 77-82.
  2. Boulton, A.J.M., F.A. Gries and J.A. Jervell, 1998. Guidelines for the diagnosis and outpatient management of diabetic peripheral neuropathy. Diabetic Med., 15: 508-514.
  3. Said, G., 2007. Diabetic neuropathy: A review. Clin. Pract. Neurol., 3: 331-340.
  4. Sato, A., Y. Sato and H. Suzuki, 1985. Aging effects on conduction velocities of myelinated and unmyelinated fibers of peripheral nerves. Lett., 53: 15-20.
  5. Felitsyn, N., P.W. Stacpoole and L. Notterpek, 2007. Dichloroacetate causes reversible demyelination in vitro: Potential mechanism for its neuropathic effect. Neurochem., 100: 429-436.
  6. Faris M Altaf , 2017. Quantitative Study of the Effect of Progesterone on the Diabetic Sural Nerves in Rats. J. Nutr., 16: 906-913.
  7. Cai, W., Y. Zhu, K. Furuya, Z. Li, M. Sokabe and L. Chen, 2008. Two different molecular mechanisms underlying progesterone neuroprotection against ischemic brain damage. Neuropharmacology, 55: 127-138.