Effects of cannabinoid (CBD) on blood brain barrier permeability after brain injury in rats

Jiang, Hong-Yan; Hengxi, Li; Cao, Yan; Zhang, Ruilin; Zhou, Lei; Zhou, Ying; Zeng, Xiaofeng; Wu, Jan‐Jan; Wu, Douwei; Wu, Deye; Guo, Xia; Li, Xiaowen; Wu, Haiying; Li, Ping

doi:10.1016/j.brainres.2021.147586

Cited by 29 publications

(22 citation statements)

References 73 publications

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“…Concomitantly, it reduced the protein levels of some pro-inflammatory cytokines and increased the expression of claudin-5 and occludin, which are tight junction proteins. CBD administration improved the integrity and permeability of the BBB and reduced edema in the brain after traumatic brain injury [ 55 ]. Cannabis also had a beneficial effect on HIV-associated BBB injury.…”

Section: Introductionmentioning

confidence: 99%

Exploring the Potential of Cannabinoid Nanodelivery Systems for CNS Disorders

et al. 2023

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Cannabinoids have a major therapeutic value in a variety of disorders. The concepts of cannabinoids are difficult to develop, but they can be used and are advantageous for a number of diseases that are not sufficiently managed by existing treatments. Nanoconjugation and encapsulation techniques have been shown to be effective in improving the delivery and the therapeutic effectiveness of drugs that are poorly soluble in water. Because the bioavailability of cannabinoids is low, the challenge is to explore different administration methods to improve their effectiveness. Because cannabinoids cross the blood-brain-barrier (BBB), they modify the negative effects of inflammatory processes on the BBB and may be a key factor in the improvement of BBB function after ischemic disease or other conditions. This review discusses various types of cannabinoid administration, as well as nanotechnologies used to improve the bioavailability of these compounds in CNS diseases.

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Section: Introductionmentioning

confidence: 99%

Exploring the Potential of Cannabinoid Nanodelivery Systems for CNS Disorders

et al. 2023

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“…It has been reported that inflammation of the central nervous system exacerbates the blood-brain barrier permeability and reduces tight junctional protein expression (McColl et al, 2008). In many nervous system diseases, secondary pathophysiological changes occur in the central nervous system after blood-brain barrier injuries, such as brain edema, elevated intracranial pressure, and internal environment disorder, further aggravating the neurological damage (Laval et al, 2018;Sun et al, 2018;Jiang et al, 2021;Jiao-Yan et al, 2021). Our data showed no blood-brain barrier leakage after the PRV challenge.…”

Section: Discussionmentioning

confidence: 44%

The Immunity Protection of Central Nervous System Induced by Pseudorabies Virus DelgI/gE/TK in Mice

Wei

Zhao

et al. 2022

Front. Microbiol.

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Based on a variant strain, we constructed a gE/gI/TK-deleted pseudorabies virus (PRV). A total of 18 female mice were randomized to a vaccination group to receive PRV XJ delgE/gI/TK, a vehicle group to receive Dulbecco’s modified Eagle’s medium, and a mock group to confirm the protection of PRV delgE/gI/TK on the central nervous system in mice. Subsequently, the vaccination and vehicle groups were infected with PRV XJ. The mice in the vehicle group showed more severe neurological symptoms and higher viral loads than those in the vaccination group. The exudation of Evans blue and the expression of tight junction protein showed no difference in all groups. HE staining showed vacuolar neuronal degeneration in the vehicle group brain, but no tissue lesions were observed in the vaccination group. TNF-α, IL-6, and synuclein were upregulated in the brain of mice in the vehicle group, while those were inhibited among mice in the vaccination group. IFN-β, IFN-γ, ISG15, Mx1, and OAS1 showed no difference in the brain between the vaccination and vehicle groups. In addition, TNF-α and IL-6 were inhibited, and antiviral factors were increased in the intestine of the mice in the vaccination group compared to those in the vehicle group. Our study showed that PRV XJ delgE/gI/TK inhibited neurological damage and the inflammation of the intestine and brain induced by PRV and activated the innate immunity of the intestine.

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“…The decreased TBI-induced acute over-release of glutamate in animals pretreated with CBD can result in lower excitotoxicity and long-term protective effects after trauma [87,88]. The observed long-term protective effects after TBI may be explained since CBD induces anti-inflammatory effects mediated by low expression of TNFα, NF-κB IL-1β, GFAP, and AQP4 and an improved BBB viability [31,89]. In addition, CBD reduces the expression of proapoptotic proteins BCL-2/Bax, and caspase-3, increasing the activity of antioxidant enzymes such as superoxide dismutase and catalase [90].…”

Section: Discussionmentioning

confidence: 99%

Cannabidiol Reduces Short- and Long-Term High Glutamate Release after Severe Traumatic Brain Injury and Improves Functional Recovery

et al. 2022

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This study aimed to determine if orally administered cannabidiol (CBD) lessens the cortical over-release of glutamate induced by a severe traumatic brain injury (TBI) and facilitates functional recovery. The short-term experiment focused on identifying the optimal oral pretreatment of CBD. Male Wistar rats were pretreated with oral administration of CBD (50, 100, or 200 mg/kg) daily for 7 days. Then, extracellular glutamate concentration was estimated by cortical microdialysis before and immediately after a severe TBI. The long-term experiment focused on evaluating the effect of the optimal treatment of CBD (pre- vs. pre- and post-TBI) 30 days after trauma. Sensorimotor function, body weight, and mortality rate were evaluated. In the short term, TBI induced a high release of glutamate (738% ± 173%; p < 0.001 vs. basal). Oral pretreatment with CBD at all doses tested reduced glutamate concentration but with higher potency at when animals received 100 mg/kg (222 ± 33%, p < 0.01 vs. TBI), an effect associated with a lower mortality rate (22%, p < 0.001 vs. TBI). In the long-term experiment, the TBI group showed a high glutamate concentration (149% p < 0.01 vs. SHAM). In contrast, animals receiving the optimal treatment of CBD (pre- and pre/post-TBI) showed glutamate concentrations like the SHAM group (p > 0.05). This effect was associated with high sensorimotor function improvement. CBD pretreatment, but not pre-/post-treatment, induced a higher body weight gain (39% ± 2.7%, p < 0.01 vs. TBI) and lower mortality rate (22%, p < 0.01 vs. TBI). These results support that orally administered CBD reduces short- and long-term TBI-induced excitotoxicity and facilitated functional recovery. Indeed, pretreatment with CBD was sufficient to lessen the adverse sequelae of TBI.

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Effects of cannabinoid (CBD) on blood brain barrier permeability after brain injury in rats

Cited by 29 publications

References 73 publications

Exploring the Potential of Cannabinoid Nanodelivery Systems for CNS Disorders

Exploring the Potential of Cannabinoid Nanodelivery Systems for CNS Disorders

The Immunity Protection of Central Nervous System Induced by Pseudorabies Virus DelgI/gE/TK in Mice

Cannabidiol Reduces Short- and Long-Term High Glutamate Release after Severe Traumatic Brain Injury and Improves Functional Recovery

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