ION-CCI模型大鼠三叉神经节中IL-17变化
|
摘要
目的检测采用眶下神经压迫术(ION-CCI)制备大鼠三叉神经痛(TN)模型中三叉神经节(TG)内白细胞介素17(IL-17)蛋白及IL-17A的mRNA表达量的变化。方法随机将成年雄性SD大鼠分成两组:假手术组(sham组)和眶下神经压迫组(ION-CCI组)。使用Von Frey hair测量两组大鼠机械疼痛阈值,并通过Western blot检测TG中IL-17蛋白表达量,RT-PCR检测IL-17A mRNA表达量。结果 ION-CCI组大鼠的机械疼痛阈值较sham组显著降低,并在第14天时达到最低值(P<0.01)。ION-CCI组大鼠TG内的IL-17蛋白表达量也显著升高且高于sham组大鼠(P<0.05),第14天时检测的IL-17A mRNA表达量也高于sham组大鼠(P<0.05)。结论 IL-17在TN发生和发展中具有重要作用。
Objective To investigate the change of the expression of IL-17 protein and IL-17 A mRNA in rat trigeminal ganglion(TG) of rat trigeminal neuralgia(TN) model prepared by infraorbital nerve compression method(ION-CCI).Methods Adult male SD rats were randomly divided into two groups: sham operation group and infraorbital nerve compression group. The mechanical pain threshold was measured by Von Frey hair, and the expression of IL-17 protein in TG was detected by Western blot, and the expression of IL-17 A mRNA was detected by RT-PCR.Results The mechanical pain threshold in ION-CCI group was significantly lower than that in sham group, and reached the lowest level on the 14 th day(P<0.01). The expression of IL-17 protein in TG of rats in ION-CCI group was also significantly higher than that in sham group(P<0.05),and on the 14 th day the expression of IL-17 A mRNA was also higher than that in sham group(P<0.05).Conclusion The IL-17 plays an important role in the occurrence and development of trigeminal neuralgia.
Objective To investigate the change of the expression of IL-17 protein and IL-17 A mRNA in rat trigeminal ganglion(TG) of rat trigeminal neuralgia(TN) model prepared by infraorbital nerve compression method(ION-CCI).Methods Adult male SD rats were randomly divided into two groups: sham operation group and infraorbital nerve compression group. The mechanical pain threshold was measured by Von Frey hair, and the expression of IL-17 protein in TG was detected by Western blot, and the expression of IL-17 A mRNA was detected by RT-PCR.Results The mechanical pain threshold in ION-CCI group was significantly lower than that in sham group, and reached the lowest level on the 14 th day(P<0.01). The expression of IL-17 protein in TG of rats in ION-CCI group was also significantly higher than that in sham group(P<0.05),and on the 14 th day the expression of IL-17 A mRNA was also higher than that in sham group(P<0.05).Conclusion The IL-17 plays an important role in the occurrence and development of trigeminal neuralgia.
引文
[1] Baeten D, Baraliakos X, Braun J, et al. Anti-interleukin-17A monoclonal antibody secukinumab in treatment of ankylosing spondylitis: a randomised, double-blind, placebo-controlled trial[J]. Lancet,2013, 382(9906): 1705-13.
[2] Moynes D M, Vanner S J, Lomax A E. Participation of interleukin 17A in neuroimmune interactions[J]. Brain Behav Immun,2014, 41: 1-9.
[3] Shurin M R. Dual role of immunomodulation by anticancer chemotherapy[J]. Nat Med,2013, 19(1): 20-2.
[4] Day Y J, Liou J T, Lee C M, et al. Lack of interleukin-17 leads to a modulated micro-environment and amelioration of mechanical hypersensitivity after peripheral nerve injury in mice[J]. Pain,2014, 155(7): 1293-302.
[5] Noma N, Khan J, Chen I F, et al. Interleukin-17 levels in rat models of nerve damage and neuropathic pain[J]. Neurosci Lett,2011, 493(3): 86-91.
[6] Kim C F, Moalem-Taylor G. Interleukin-17 contributes to neuroinflammation and neuropathic pain following peripheral nerve injury in mice[J]. J Pain,2011, 12(3):370-83.
[7] Kiguchi N, Kobayashi D, Saika F, et al. Pharmacological regulation of neuropathic pain driven by inflammatory macrophages[J]. Int J Mol Sci,2017, 18(11).pii: E2296.
[8] Yao C Y, Weng Z L, Zhang J C, et al. Interleukin-17A acts to maintain neuropathic pain through activation of CaMKII/CREB signaling in spinal neurons[J]. Mol Neurobiol,2016, 53(6): 3914-26.
[9] Olechowski C J, Truong J J, Kerr B J. Neuropathic pain behaviours in a chronic-relapsing model of experimental autoimmune encephalomyelitis(EAE)[J]. Pain,2009, 141(1):156-64.
[10] Sun C, Zhang J, Chen L, et al. IL-17 contributed to the neuropathic pain following peripheral nerve injury by promoting astrocyte proliferation and secretion of proinflammatory cytokines[J]. Mol Med Rep, 2017, 15(1): 89-96.
[2] Moynes D M, Vanner S J, Lomax A E. Participation of interleukin 17A in neuroimmune interactions[J]. Brain Behav Immun,2014, 41: 1-9.
[3] Shurin M R. Dual role of immunomodulation by anticancer chemotherapy[J]. Nat Med,2013, 19(1): 20-2.
[4] Day Y J, Liou J T, Lee C M, et al. Lack of interleukin-17 leads to a modulated micro-environment and amelioration of mechanical hypersensitivity after peripheral nerve injury in mice[J]. Pain,2014, 155(7): 1293-302.
[5] Noma N, Khan J, Chen I F, et al. Interleukin-17 levels in rat models of nerve damage and neuropathic pain[J]. Neurosci Lett,2011, 493(3): 86-91.
[6] Kim C F, Moalem-Taylor G. Interleukin-17 contributes to neuroinflammation and neuropathic pain following peripheral nerve injury in mice[J]. J Pain,2011, 12(3):370-83.
[7] Kiguchi N, Kobayashi D, Saika F, et al. Pharmacological regulation of neuropathic pain driven by inflammatory macrophages[J]. Int J Mol Sci,2017, 18(11).pii: E2296.
[8] Yao C Y, Weng Z L, Zhang J C, et al. Interleukin-17A acts to maintain neuropathic pain through activation of CaMKII/CREB signaling in spinal neurons[J]. Mol Neurobiol,2016, 53(6): 3914-26.
[9] Olechowski C J, Truong J J, Kerr B J. Neuropathic pain behaviours in a chronic-relapsing model of experimental autoimmune encephalomyelitis(EAE)[J]. Pain,2009, 141(1):156-64.
[10] Sun C, Zhang J, Chen L, et al. IL-17 contributed to the neuropathic pain following peripheral nerve injury by promoting astrocyte proliferation and secretion of proinflammatory cytokines[J]. Mol Med Rep, 2017, 15(1): 89-96.