THC significantly reduced brain inflammation and oxidative damage in rats exposed to a high-fructose diet, according to a new study that found the cannabinoid helped counter several harmful biochemical changes associated with excessive sugar consumption.
Published October 17 in Naunyn-Schmiedeberg’s Archives of Pharmacology, the study was conducted by researchers from Istanbul Kent University, Demiroglu Bilim University and Istanbul University-Cerrahpaşa in Türkiye. Researchers examined whether delta-9-tetrahydrocannabinol (THC), marijuana’s primary psychoactive compound, could protect brain tissue against inflammation and oxidative stress triggered by prolonged fructose exposure.
The experiment involved 32 Sprague-Dawley rats divided into four groups. One received a standard diet, another consumed drinking water containing 10% fructose for 12 weeks, a third received THC without fructose exposure, and the fourth received both fructose and THC. Animals treated with THC received 1.5 milligrams per kilogram of body weight daily during the final four weeks.
Researchers analyzed brain tissue for markers of protein and lipid oxidation, mitochondrial activity and inflammation.
Rats exposed to the high-fructose diet showed significant increases in several indicators of oxidative damage, including advanced oxidation protein products, malondialdehyde and advanced glycation end products. They also exhibited reduced levels of total thiols, compounds that help protect cells against oxidative damage.
The high-fructose diet also increased the activity of several inflammation-related genes, including IL-6, IL-1β, TNF-α and NF-κB. These genes are involved in inflammatory signaling and immune responses within the body.
THC treatment significantly reduced markers of oxidative damage and lowered the expression of the inflammation-related genes examined. Researchers also observed reductions in altered NADH and FAD fluorescence measurements, which are associated with mitochondrial redox activity and cellular energy processes.
The analysis found strong positive correlations between inflammatory gene expression and oxidative stress markers, indicating that greater oxidative damage was closely associated with increased inflammatory activity in brain tissue.
The findings suggest THC may help counter some of the harmful neurological effects associated with prolonged exposure to high levels of dietary fructose, particularly those involving inflammation, oxidative damage and mitochondrial function.
The researchers concluded that THC administration was associated with significant reductions in high-fructose diet-induced oxidative stress and neuroinflammatory signaling. The experiment measured biochemical changes in rats rather than cognitive performance or clinical outcomes in humans.
