Abstract
Treatment of painful neuromas remains a challenge and the mechanism of neuroma-associated pain is not yet fully understood. In this study, we aimed to observe the expression of alpha smooth muscle actin (α-SMA) in traumatic neuromas and to investigate its possible roles in the cause of neuropathic pain in a rat model. The rat sciatic nerve was used and the experiment was divided into two parts. In part I, our results showed significantly higher levels of α-SMA and the pain marker c-fos in the autotomy group than in the no-autotomy group. In part II, the expression of α-SMA in neuromas was down- and up-regulated using SB-431542 and GW9662, respectively. A significant correlation between autotomy scores and the expression level of α-SMA was found (R = 0.957; p < 0.001) and the expression level of α-SMA was positively related to the autotomy scores (R2 = 0.915, p < 0.001). We concluded that the expression of α-SMA plays certain roles in the neuroma-associated pain, either as a direct cause of pain or as an indirect marker of existence of local mechanical stimuli. Our findings may provide new insights into the development of new treatment modalities for the management of intractable painful neuromas.
Highlights
ObjectivesWe aimed to observe the expression of alpha smooth muscle actin (α-SMA) in traumatic neuromas and to investigate its possible roles in the cause of neuropathic pain in a rat model
Values are expressed as the mean ± standard error of the mean (SEM), n = 6 per group. *P < 0.05 versus the no-autotomy group
The neuroma in the SB-431542 group had a lower Weight ratios (WR) (0.48 ± 0.079) than in the control group (0.61 ± 0.049) while the highest WR was seen in the GW9662 group (0.72 ± 0.041); the differences in WR were significant among the three groups (SB-431542 vs. control group, p = 0.002; GW9662 group vs. control group, p = 0.008; SB-431542 vs. GW9662, p < 0.001)
Summary
We aimed to observe the expression of alpha smooth muscle actin (α-SMA) in traumatic neuromas and to investigate its possible roles in the cause of neuropathic pain in a rat model. We aim to further investigate the significance of α -SMA expression in the traumatic neuroma and potential role in the mechanism of neuropathic pain in a rat model
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