| 薛继娇,冯 慧,孟祥君,李 帅,席富强.BNP/NPR-A/BKCa信号通路在大鼠神经痛形成中的作用及机制研究[J].,2023,(15):2817-2821 |
| BNP/NPR-A/BKCa信号通路在大鼠神经痛形成中的作用及机制研究 |
| The Role and Mechanism of BNP/NPR-A/BKCa Signaling Pathway in Neuralgia Formation in Rats |
| 投稿时间：2023-02-13 修订日期：2023-03-10 |
| DOI：10.13241/j.cnki.pmb.2023.15.003 |
| 中文关键词: BNP/NPR-A/BKCa信号通路 大鼠 神经痛 |
| 英文关键词: BNP/NPR-A/BKCa signal pathway Rat Neuralgia |
| 基金项目:内蒙古自治区教育厅学校科学研究项目（NJZY22085） |
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| 中文摘要: |
| 摘要 目的：探讨BNP/NPR-A/BKCa信号通路在大鼠神经痛形成中的作用及机制研究。方法：选取SPF级大鼠作为研究对象，并构建神经痛病理性疼痛大鼠模型。并分为空白对照组、假手术组、A组（20 ng/mL BNP梢内注射）、B组（50 ng/mL BNP梢内注射）和C组（100 ng/mL BNP梢内注射）。采用qRT-PCR和Western blot检测NPR-A和BKCa的mRNA和蛋白表达水平。采用ELISA法检查炎症因子。全细胞膜片钳技术检测痛觉神经元BKCa通道电流；对大鼠进行机械性痛觉过敏测试和温度性痛觉敏感测试。结果：与空白组相比，模型组、A、B和C组PWT和PWL明显更低（P＜0.05）；与模型组相比，A、B和C组PWT和PWL明显更高，且C组大于B和A组，B组大于A组（P＜0.05）。与空白组相比，模型组NPR-A的蛋白和mRAN水平明显更高，而BKCa-α明显更低（P＜0.05）；与模型组相比，A、B和C组NPR-A和BKCa-α的蛋白和mRNA明显更高，且C组大于B和A组，B组大于A组（P＜0.05）。各电压水平，与空白组相比，模型组、A、B和C组BKCa-α电流水平明显更低（P＜0.05）；与模型组相比，A、B和C组BKCa-α电流水平明显更高，且C组大于B和A组，B组大于A组（P＜0.05）。与空白组相比，模型组、A、B和C组TNF-α、IL-6和IL-18水平明显更高（P＜0.05）；与模型组相比，A、B和C组TNF-α、IL-6和IL-18水平明显更低，且C组小于B和A组，B组小于A组（P＜0.05）。结论：靶向上调BNP的表达水平可增加BKCa的表达及BKCa电流，同时BNP的表达上调还有助于抑制炎症因子水平，从而达到多途径缓解疼痛的目的。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the role and mechanism of BNP/NPR-A/BKCa signaling pathway in neuralgia formation in rats. Methods: SPF rats were selected as research subjects and pathologic pain rat model of neuralgia was established. They were divided into blank control group, sham operation group, group A (20 ng/mL BNP injection), group B (50 ng/mL BNP injection) and group C (100ng/ml BNP injection). The mRNA and protein expression levels of NPR-A and BKCa were detected by qRT-PCR and Western blot. Inflammatory factors were examined by ELISA. BKCa channel currents of pain-sensing neurons were detected by whole-cell patch clamp technique. Mechanical hyperalgesia and temperature hyperalgesia were tested in rats. Results: Compared with blank group, PWT and PWL in model group, groups A, B and C were lower (P<0.05). Compared with the model group, the PWT and PWL in groups A, B and C were higher, and the PWT and PWL in group C were higher than those in groups B and A, and the PWL in group B was higher than that in group A (P<0.05). Compared with blank group, the level of NPR-A protein and mRAN was higher in model group, while the level of BKCa-α was lower (P<0.05). Compared with model group, the protein and mRNA of NPR-A and BKCa-α in groups A, B and C were higher, and group C was higher than that in groups B and A, and group B was higher than that in group A (P<0.05). Compared with blank group, the current level of BKCa-α in model group, groups A, B and C was lower (P<0.05). Compared with the model group, the current level of BKCa-α in groups A, B and C was significantly higher, and group C was higher than that in groups B and A, and group B was higher than that in group A (P<0.05). Compared with blank group, the levels of TNF-α, IL-6 and IL-18 in model group, groups A, B and C were significantly higher (P<0.05). Compared with model group, the levels of TNF-α, IL-6 and IL-18 in groups A, B and C were significantly lower, and group C was lower than that in groups B and A, and group B was lower than that in group A (P<0.05). Conclusion: Targeted up-regulation of BNP expression level can increase the expression of BKCa and the current of BKCa. Meanwhile, the up-regulation of BNP expression can also help to inhibit the level of inflammatory cytokines, so as to achieve the purpose of pain relief in multiple ways. |
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