| 引用本文: |
罗小精, 田楚宁, 展立芬, 李芊, 梁柔筠, 林志坚, 卓越, 许明, 张泓.电针对脊髓损伤大鼠肠道动力及直肠Ca2+/CaM/MLCK信号通路的影响[J].湖南中医药大学学报,2025,45(5):862-868[点击复制] |
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| 电针对脊髓损伤大鼠肠道动力及直肠Ca2+/CaM/MLCK信号通路的影响 |
| 罗小精,田楚宁,展立芬,李芊,梁柔筠,林志坚,卓越,许明,张泓 |
| (湖南中医药大学针灸推拿与康复学院, 湖南 长沙 410208) |
| 摘要: |
| 目的 观察电针对脊髓损伤大鼠直肠组织钙离子（Ca2+）、钙调蛋白(CaM）以及肌球蛋白轻链激酶（MLCK）的影响，探讨电针改善脊髓损伤后大鼠肠道动力的潜在机制。方法 42只成年雌性SD大鼠中随机选取10只作为假手术组，剩余32只大鼠进行T10椎体下脊髓完全横断手术以建立脊髓损伤模型，将评估成模的20只大鼠随机分为模型组和电针组，每组10只。电针组从造模后第19天给予电针干预，20 min/次，1 次/d，连续治疗7 d；假手术组和模型组仅捆绑，不干预。观察各组大鼠治疗前后一般状况、体质量变化、粪便含水量、肠道推进率，采用离体直肠平滑肌收缩试验观察直肠平滑肌的收缩性，采用比色法检测直肠组织Ca2+浓度，并通过Western blot检测直肠平滑肌组织CaM及MLCK蛋白表达水平。结果 干预后，与假手术组相比，模型组大鼠反应迟钝、精神状态差、进食饮水减少，体质量、粪便含水量和肠道推进率均降低（P＜0.05），离体直肠平滑肌条自发性收缩的张力的最大值、最小值、幅度及收缩频率均下降（P＜0.05），直肠组织Ca2+浓度降低（P＜0.05），直肠平滑肌组织CaM及MLCK蛋白表达水平降低（P＜0.05）；与模型组相比，电针组大鼠精神状态稍好、进食饮水增加，体质量、粪便含水量和肠道推进率均升高（P＜0.05），离体直肠平滑肌条自发性收缩的张力的最大值、最小值、幅度及收缩频率均升高（P＜0.05），直肠组织Ca2+浓度升高（P＜0.05），直肠平滑肌组织CaM、MLCK蛋白表达水平升高（P＜0.05）。结论 电针能调节脊髓损伤后大鼠的肠道动力，其效应机制可能与调控Ca2+/CaM/MLCK信号通路信号有关。 |
| 关键词: 脊髓损伤 肠道动力 电针 钙离子 钙调蛋白 肌球蛋白轻链激酶 |
| DOI：10.3969/j.issn.1674-070X.2025.05.011 |
| 投稿时间：2025-01-07 |
| 基金项目:国家自然科学基金面上项目（82274666）；湖南中医药大学学科建设“揭榜挂帅”项目（22JBZ013）；湖南中医药大学研究生创新项目（2024CX167）；湖南中医药大学本科生科研创新基金项目（2024BKS124）。 |
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| Effects of electro-acupuncture on intestinal motility and rectal Ca2+/CaM/MLCK signaling pathway in rats with spinal cord injury |
| LUO Xiaojing, TIAN Chuning, ZHAN Lifen, LI Qian, LIANG Rouyun, LIN Zhijian, ZHUO Yue, XU Ming, ZHANG Hong |
| (School of Acupuncture-moxibustion, Tuina and Rehabilitation, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China) |
| Abstract: |
| Objective To observe the effects of electro-acupuncture (EA) on calcium ion (Ca2+), calmodulin (CaM), and myosin light-chain kinase (MLCK) in rectal tissue of rats with spinal cord injury (SCI), so as to explore the potential mechanism of EA in improving intestinal motility of SCI rats. Methods Among 42 adult female SD rats, ten were randomly selected as the sham-operated group, while the remaining 32 rats underwent complete transection of the spinal cord at the T10 spinal segment to establish a SCI model. Twenty successfully modeled rats were randomly divided into model group and EA group, with ten rats in each group. The EA group was given EA intervention starting from day 19 after modeling, 20 minutes per session, once a day, for seven consecutive days. The sham-operated and model groups underwent only restraint without intervention. The general condition, body weight change, fecal water content, and intestinal propulsion rate of rats were observed before and after treatment in groups. The contractility of rectal smooth muscle was observed by in vitro rectal smooth muscle contraction test. The Ca2+ concentration of rectal tissue was determined by colorimetry, and the expression levels of CaM and MLCK proteins in rectal smooth muscle tissue were checked by Western blot. Results After intervention, compared with the sham-operated group, the model group exhibited lethargy, poor mental state, reduced food and water intake, body weight, fecal water content, and intestinal propulsion rate (P<0.05). Spontaneous contractions of isolated rectal smooth muscle strips showed reduced maximal/minimal tension, amplitude, and frequency (P<0.05). The Ca2+ concentration in rectal tissue (P<0.05) and the CaM and MLCK protein expression levels in rectal smooth muscle tissue decreased (P<0.05). Compared with the model group, the EA group showed improved mental state, increased food and water intake, and elevated body weight, fecal water content, and intestinal propulsion rate (P<0.05). Spontaneous contractions of rectal smooth muscle strips demonstrated enhanced maximal/minimal tension, amplitude, and frequency (P<0.05), along with increased rectal tissue Ca2+ concentration (P<0.05) and CaM/MLCK protein expression levels (P<0.05). Conclusion EA can improve intestinal motility in SCI rats and its mechanism may be related to the regulation of Ca2+/CaM/MLCK signaling pathway. |
| Key words: spinal cord injury intestinal motility electro-acupuncture calcium ion calmodulin myosin light-chain kinase |
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