A new study being published in this month’s issue of the journal Experimental Neurology, and published online this week by the U.S. National Institute of Health, has found that stimulation of the body’s cannabinoid receptors – such as through the consumption of cannabis – attenuates early brain injury.
For the study, researchers evaluated whether a cannabinoid receptor type 2 (CB2R) agonist (something which cannabis is) attenuates early brain injury (EBI) after SAH [subarachnoid hemorrhage], and “whether CB2R stimulation reduces pro-apoptotic caspase-3 via up-regulation of cAMP response element-binding protein (CREB)-Bcl-2 signaling pathway.”
“Male Sprague Dawley rats” were subjected to SAH by endovascular perforation, and received a CB2R agonist an hour afterward.
After doing so, “Neurological deficits and brain water content were evaluated at 24 hours after SAH. Western blot was performed to quantify phosphorylated CREB (pCREB), Bcl-2, and cleaved caspase-3 levels. Neuronal cell death was evaluated with terminal deoxynucleotidyl transferase-mediated uridine 5′-triphosphate-biotin nick end-labeling staining. Additionally, CREB siRNA was administered to manipulate the proposed pathway.”
It was found that the CB2R agonist “improved neurological deficits and reduced brain water content in left hemisphere 24 hours after SAH.” It also “significantly increased activated CREB (pCREB) and Bcl-2 levels and significantly decreased cleaved caspase-3 levels in left hemisphere 24 hours after SAH.”
Researchers conclude; “TUNEL positive neurons in the cortex were reduced [with the CB2R treatment]. Thus, CB2R stimulation attenuated EBI after SAH possibly through activation of pCREB-Bcl-2 pathway.
The study was conducted by researchers at the Loma Linda University Department of Physiology and Department of Anesthesiology.