This study investigated the antinociceptive potential of cannabidiol (CBD) in male and female Wistar rats. The assessment and analysis included tail withdrawal to thermal stimulation (tail flick test) and mechanical allodynia induced by plantar incision injury (von Frey test). CBD reduced acute thermal sensitivity in uninjured animals and post-operative mechanical allodynia in males and females. In the tail flick test, CBD 30 mg/kg i.p. was required to induce antinociception in males. During the proestrus phase, females did not show a statistically significant antinociceptive response to CBD treatment despite a noticeable trend. In contrast, in a separate group of rats tested during the late diestrus phase, antinociception varied with CBD dosage and time. In the post-operative pain model, CBD at 3 mg/kg decreased mechanical allodynia in males. Similarly, this dose reduced allodynia in females during proestrus. However, in females during late diestrus, the lower dose of CBD (0.3 mg/kg) reduced mechanical allodynia, although the latency to onset of the effect was slower (90 min). The effectiveness of a 10-fold lower dose of CBD during the late diestrus stage in females suggests that ovarian hormones can influence the action of CBD. While CBD has potential for alleviating pain in humans, personalized dosing regimens may need to be developed to treat pain in women.
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http://dx.doi.org/10.1016/j.bbr.2023.114793 | DOI Listing |
Acta Neurobiol Exp (Wars)
January 2025
Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Piperine is an amide alkaloid isolated from the black pepper plant. This study examined the pain‑relieving activity of piperine against paclitaxel (PTX)‑induced neuropathy. Male mice were divided into 6 groups: Sham‑operated group (remained intact), PTX group (PTX‑treated mice receiving normal saline), PTX+ piperine 10, 25, and 50 mg/kg groups (PTX‑treated mice receiving piperine) and positive control group (PTX‑treated mice receiving imipramine 10 mg/kg).
View Article and Find Full Text PDFExtracell Vesicles Circ Nucl Acids
December 2024
Department of Diagnostic and Biological Sciences, University of Minnesota, Minneapolis, MN 55455, USA.
The effective management of cancer pain continues to be a challenge because of our limited understanding of cancer pain mechanisms and, in particular, how cancer cells interact with neurons to produce pain. In a study published in , Inyang used a mouse model of human papillomavirus (HPV1)-induced oropharyngeal squamous cell carcinoma to show a role for cancer cell-derived extracellular vesicles (cancer sEVs) in cancer pain. They found that inhibiting the release of sEVs reduced spontaneous and evoked pain behaviors, and that pain produced by sEVs is due to activation of TRPV1 channels.
View Article and Find Full Text PDFOsteoarthr Cartil Open
March 2025
Department of Orthopedic Surgery, Mayo Clinic, Rochester, MN, USA.
Objective: Osteoarthritis is a chronic, debilitating disease that causes long-term pain and immobility. Germline deletion of Phlpp1 or administration of small molecules that inhibit Phlpp1 prevents post-traumatic osteoarthritis (PTOA) in mice. However, the chondrocyte-intrinsic role of Phlpp1 in PTOA progression is unknown.
View Article and Find Full Text PDFIBRO Neurosci Rep
December 2024
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Previous investigations have revealed the role of GABAergic and serotonergic systems in the modulation of pain behavior. This research aimed to examine the effects of intracerebroventricular (i.c.
View Article and Find Full Text PDFActa Pharm Sin B
December 2024
Department of Translational Neuroscience, Jing'an District Centre Hospital of Shanghai, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai 200032, China.
Spinal microglia and astrocytes are both involved in neuropathic and inflammatory pain, which may display sexual dimorphism. Here, we demonstrate that the sustained activation of spinal astrocytes and astrocyte-derived interleukin (IL)-17A promotes the progression of mouse bone cancer pain without sex differences. Chemogenetic or pharmacological inhibition of spinal astrocytes effectively ameliorates bone cancer-induced pain-like behaviors.
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