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From left to right, the researchers Arnau Hervera and José Antonio del Río (Photo: IBEC).

The oxidation process favours recovery after a spine injury

The inflammatory response and oxidation after a nerve injury could favour the regeneration of axons (prolongation of neurons). This is the most relevant conclusion of a pre-clinical study published in the journal Nature Cell Biology, with the participation of researchers from the University of Barcelona (UB) and the Institute for Bioengineering of Catalonia (IBEC) at the Barcelona Science Park. This work, carried out in collaboration with scientifics from the Imperial College London, suggests that the indiscriminate use of antioxidant therapies on nerve injuries should be examined, since these could block the body’s own regenerative response.


The common drugs to ease the effects of a spine cord injury or an injury in the nervous system are anti-inflammatories and antioxidants. When a nerve is injured, a process of inflammation occurs and the immune system gets activated –it sends macrophages so they act on the damaged area- and there is a high level of oxidation, which affects the membrane and DNA of some neurons, and can cause cell death. 

Although you’d think that inhibiting the inflammatory response and oxidation after injury would avoid this damage, the team of researchers discovered have discovered that oxidation can actually promote the regeneration of axons after a nerve injury.

The study focuses on the unchained mechanisms of a preconditioning nerve injury, associated with high oxidation levels (reactive oxygen species, ROS). “When there has been a prior lighter injury in the nervous system, the recovery after an acute injury proves to be more effective”, says researcher Arnau Hervera (IBEC), first author of the study. “We could therefore think this mechanism is similar to the vaccines, preparing the immune system for an attack, that is, like a cell memory”, he adds.

According to Professor José Antonio del Río (UB, UBNeuro and IBEC), “a conditioning injury wouldn’t be useful therapeutically. However, if we understand the mechanisms that lie behind –basically, how this oxidation works-, we can control and improve the regeneration after spine injuries”.

The new study identifies macrophages as the key factors of signalling –through ROS- to enhance the regeneration of the injured axons. The study, carried out in collaboration with the team led by Professor Simone di Giovanni, from the Imperial College London, could serve to inspire the design of new drugs to activate spinal regeneration regulating the pre-injury oxidation process. Moreover, the indiscriminate use of antioxidant therapies on nerve injuries should be examined, since these could block the body’s own regenerative response.

►Reference article: 
A. Hervera, F. De Virgiliis, I. Palmisano, L. Zhou, E. Tantardini, G. Kong, T. Hutson, M. C. Danzi, R. Ben-Tov Perry, C. X. C. Santos, A. N. Kapustin, R. A. Fleck, J. A. Del Río, T. Carroll, V. Lemmon, J. L. Bixby, A. M. Shah, M. Fainzilber and S. Di Giovanni. Nature Cell Biology “Reactive oxygen species regulate axonal regeneration through the release of exosomal NADPH2 oxidase complexes into injured axons“. Nature Cell Biology. Feb 2018, Vol. 20. Doi:10.1038/s41556-018-0039-x

►More information: IBEC website [+]