By Anthony Martinelli

Cannabinoids may help people recover from a spinal cord injury, according to a new study.

is being published in the journal Brain Research, and has been e-published ahead of print by the U.S. National Institute of Health.

“The endocannabinoid system, including its receptors (CB1 and CB2), act as neuroprotective and immunomodulatory modulators in SCI [spinal cord injury]”, states the study’s abstract. “WIN55212-2, an agonist for CB1 and CB2 receptors, has been demonstrated with anti-inflammatory and anti-apoptotic effects in multiple neurological diseases.” Therefore, the present study “aimed to investigate whether WIN55212-2 could promote functional recovery after traumatic SCI via inhibition of the GAPDH/Siah1 signaling.”

For the study, the traumatic SCI “was induced by dropping a 10-g impactor from 25 mm on the dorsal surface of T9 and T10.” The results “showed that WIN55212-2 alleviated the activation of GAPDH/Siah1 signaling pathway after SCI, as indicated by the reduction in GAPDH nuclear expression, GAPDH-Siah1 complex formation and iNOS protein expression.’

Furthermore, WIN55212-2 “reduced apoptosis, production of IL-1β and TNF-α and activation of NF-κB signaling in the spinal cord after SCI. The behavioral tests showed that WIN55212-2 improved the functional recovery after traumatic SCI as indicated by sustained increase in the locomotor scores.

In conclusion, the study “indicates that, WIN55212-2 improves the functional recovery after SCI via inhibition of GAPDH/Siah1 cascades in a CB2 receptor dependent manner, indicative of its therapeutic potential for traumatic SCI or other traumatic conditions.”

The full study, conducted by researchers at Fourth Military Medical University and Shaanxi Provincial People’s Hospital, both in China,, can be found by clicking here.

The results of the study are similar to that of a 2015 study – also published by the National Institute of Health – which found that “post-injury CB1R agonism can improve SCI outcome and also indicate marked attenuation of MMP-9 proteolytic enzyme activity as a biochemical mechanism.”

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