CB1 Activation Helps Speed Wound Healing, Reports Study
- Activation of cannabinoid receptor 1 (CB1) enhances key wound-healing processes in human skin fibroblasts, increasing cell proliferation, differentiation, and production of wound repair proteins like α-SMA, N-cadherin, and vimentin.
- CB1 activation boosts fibroblast migration and the synthesis of structural components critical for tissue repair, including type I and III collagen and fibronectin; these effects were blocked by the CB1 antagonist AM251, confirming CB1 specificity.
- In mice with acute skin wounds, treatment with a CB1 agonist accelerated wound closure, increased expression of repair proteins, and resulted in thicker epidermal and dermal layers at the wound site.
- The study suggests that CB1 activation promotes fibroblast activity and tissue remodeling, indicating CB1 agonists could be promising candidates for developing new wound-healing therapies.
Researchers from Hallym University and Eulji University in the Republic of Korea report that activating cannabinoid receptor 1 (CB1) boosted several key wound-healing processes in human skin cells and accelerated wound closure in mice, according to findings published in International Journal of Molecular Sciences. CB1 is best known for its role in the nervous system, but the team focused on whether switching it on could also influence tissue repair. In lab experiments, they isolated fibroblasts from human dermis and treated the cells with a CB1 agonist called 2-arachidonyl glyceryl ether (2-AGE). Compared with untreated cells, exposed fibroblasts showed increased proliferation and signs of differentiation, along with higher levels of proteins tied to wound repair, including alpha-smooth muscle actin (α-SMA), N-cadherin and vimentin.
The researchers also reported enhanced cell migration and increased production of structural components that help rebuild damaged tissue, including type I and III collagen and fibronectin. To confirm the effect was specifically tied to CB1, they added a CB1 antagonist, AM251, which blocked 2-AGE-related increases in α-SMA, type I collagen and fibronectin.
In an animal arm of the study, the researchers created acute wounds in mice using a skin biopsy punch and treated the area with another CB1 agonist, arachidonoyl 2’-chloroethylamide (ACEA). They found ACEA treatment sped wound closure and increased expression of α-SMA, type I collagen and fibronectin in the healing tissue. The team also reported thicker epidermal and dermal layers in treated wounds.
Overall, the findings suggest CB1 activation (something done naturally via the consumption of cannabis and cannabinoids) may help drive wound repair by promoting fibroblast activity, supporting tissue remodeling and accelerating closure, pointing to CB1 agonists as potential candidates for future wound-treatment strategies.