Abstract
Trigeminal neuralgia (TN), a sudden, needle-like pain in the distribution area of the trigeminal nerve, can seriously affect the physical and mental health of patients. In chronic pain conditions including TN, increased levels of brain-derived neurotrophic factor (BDNF) may enhance pain transmission. This study compares the effect of palmatine administration on the expression of BDNF and its receptor TrkB (tropomyosin receptor kinase B) in trigeminal ganglion cells of Sprague-Dawley rats in a sham versus TN model group. Within 14 days of surgery, the mechanical allodynia threshold of the TN group was significantly lower than that of the sham group, while the TN + palmatine group had a higher mechanical pain sensitivity threshold than the TN group (p < 0.05). Real-time quantitative PCR, immunohistochemistry, and immunofluorescence showed that BDNF and TrkB expression in the TN group was higher than that in the sham group, while palmatine treatment could reverse these changes. Western blotting showed that palmatine treatment could reduce the elevated phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2) in TN rats. Thus, the BDNF/TrkB pathway may be involved in the pain transmission process of TN, and palmatine treatment may reduce pain transmission by inhibiting the BDNF/TrkB pathway and suppressing ERK1/2 phosphorylation.
Highlights
Trigeminal neuralgia (TN) is a sharp, sudden pain in the trigeminal nerve region, the largest pair of nerves in the brain
We found that palmatine treatment noticeably reduced the pain sensitivity of TN rats for 2 weeks
These results showed that the expression of Brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) mRNA in the trigeminal ganglion (TG) of TN rats was higher than those in the sham group
Summary
Trigeminal neuralgia (TN) is a sharp, sudden pain in the trigeminal nerve region, the largest pair of nerves in the brain. Pharmacological treatments, including carbamazepine, oxcarbazepine, and other anticonvulsants and antipsychotics, have achieved varying degrees of success. Their side effects and potential loss in efficacy over time has prompted the search for other drugs that can achieve more comprehensive and long-lasting pain control[2]. Carbamazepine and oxcarbazepine confer a significant risk of side effects and complications[3] Both are prohibited to primary TN patients with an atrioventricular block[4]. The study aimed to investigate whether palmatine treatment can affect the expression of BDNF/ TrkB in the trigeminal ganglion (TG) of TN model rats and its possible molecular mechanism, which may provide new insights into the prevention and treatment of TN
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