| 莫申申,张芹,张丽萍,庄小凡.滋肾清心安神汤对围绝经期抑郁模型小鼠行为学的改善作用及对神经炎症的影响[J].浙江中西医结合杂志,2025,35(12): |
| 滋肾清心安神汤对围绝经期抑郁模型小鼠行为学的改善作用及对神经炎症的影响 |
| The ameliorative effects of Zishen Qingxin Anshen Decoction on behavioral performance and neuroinflammation in a perimenopausal depression mouse model Shenshen Mo, Department of Neurology, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China |
| 投稿时间：2025-03-20 修订日期：2025-08-16 |
| DOI： |
| 中文关键词: 小鼠，围绝经期，抑郁症，滋肾清心安神汤，行为学，神经炎症 |
| 英文关键词:Mouse Perimenopause Depression Zishen Qingxin Anshen Decoction Behavior Neuroinflammation |
| 基金项目:浙江省中医药科技计划项目 |
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| 中文摘要: |
| 摘要：目的 探究滋肾清心安神汤对围绝经期抑郁模型小鼠行为学的改善作用及对神经免疫机制的影响。方法 采用随机数字表法将雌性C57小鼠随机分为5组（n=9）:对照组、模型组、盐酸帕罗西汀组（阳性对照组）、滋肾清心安神汤低剂量组（ZSQXAST-L）、滋肾清心安神汤高剂量组（ZSQXAST-H）。摘除双侧卵巢联合慢性束缚应激法建立围绝经期抑郁模型小鼠，对照组仅摘除卵巢周围脂肪组织并每日抚摸。对照组及模型组每天灌胃生理盐水，阳性对照组每日灌胃盐酸帕罗西汀药液0.01g·kg?1，ZSQXAST-L、ZSQXAST-H每日分别给予34.8g·kg?1
69.6g·kg?1药液灌胃。给药3周后检测小鼠糖水偏好、强迫游泳、旷场实验行为学表现，在体多通道记录小鼠脑电-肌电，取大脑皮层组织检测NF-κB、抗炎因子—IL-10和TGF-β、促炎因子—IL-6 和TNF-α含量。结果 与对照组相比，模型组的强迫游泳不动时间、觉醒时间比例显著高于对照组，糖水偏好比例、旷场中央活动路程、旷场实验中央滞留时间、NREM时间比例均显著降低，提示小鼠有焦虑抑郁及睡眠减少的情况，给予帕罗西汀作为阳性药物干预后小鼠的焦虑抑郁行为均减轻，但睡眠情况没有改善。给予ZSQXAST低剂量和高剂量干预均能显著改善焦虑抑郁行为和睡眠情况。相比于对照组，模型组小鼠大脑皮层中NF-κB、IL-6 、TNF-α含量均显著升高，IL-10和TGF-β水平下降，ZSQXAST-L干预后NF-κB、IL-6 、TNF-α含量下调，IL-10和TGF-β水平得以改善。
结论 滋肾清心安神汤能显著改善围绝经期抑郁模型小鼠的抑郁行为、焦虑行为及睡眠结构，并通过上调抗炎因子—IL-10和TGF-β、下调促炎因子—IL-6 和TNF-α含量调节神经炎症。 |
| 英文摘要: |
| ABSTRACT Objective To investigate the ameliorative effects of Zishen Qingxin Anshen Decoction (ZSQXAST) on behavioral performance and its impact on neuroimmune mechanisms in a perimenopausal depression mouse model. Methods Female C57 mice were randomly assigned to five groups (n=9) using a random number table: control group, model group, paroxetine hydrochloride group (positive control), low-dose ZSQXAST group (ZSQXAST-L), and high-dose ZSQXAST group (ZSQXAST-H). The perimenopausal depression model was established by bilateral ovariectomy combined with chronic restraint stress, while the control group underwent only periovarian fat removal with daily gentle handling. The control and model groups were given normal saline by gavage daily, the positive control group received paroxetine hydrochloride (0.01g·kg?1) by gavage, and the ZSQXAST-L and ZSQXAST-H groups were administered 34.8 g·kg?1 and 69.6 g·kg?1 of ZSQXAST, respectively, by gavage. After three weeks of administration, behavioral tests including sucrose preference test, forced swimming test, and open field test were conducted. In vivo multi-channel recordings were used to assess electroencephalogram-electromyogram (EEG-EMG) sleep parameters. Enzyme-linked immunosorbent assay (ELISA) was performed on cortical tissues to measure the levels of NF-κB, anti-inflammatory cytokines (IL-10 and TGF-β), and pro-inflammatory cytokines (IL-6 and TNF-α). Results Compared with the control group, the model group showed a significantly increased immobility time in the forced swimming test and a higher proportion of wakefulness time. Meanwhile, the sucrose preference ratio, distance traveled in the central area of the open field test, central retention time in the open field test, and the proportion of NREM sleep time were significantly reduced, indicating that the mice exhibited anxiety, depression, and reduced sleep. After intervention with paroxetine as a positive control drug, the anxiety and depression behaviors of the mice were alleviated, but sleep conditions did not improve. Low-dose and high-dose interventions with ZSQXAST Decoction significantly improved both anxiety and depression behaviors as well as sleep conditions. Compared with the control group, the levels of NF-κB, IL-6, and TNF-α in the cerebral cortex of the model group were significantly increased, while the levels of IL-10 and TGF-β were decreased. After intervention with ZSQXAST Decoction, the levels of NF-κB, IL-6, and TNF-α were downregulated, and the levels of IL-10 and TGF-βwere improved. Conclusion ZSQXAST Decoction significantly improves depressive and anxiety-like behaviors as well as sleep structure in perimenopausal depression model mice. Its mechanism may be related to the regulation of neuroinflammation through the upregulation of anti-inflammatory cytokines IL-10 and TGF-β and the downregulation of pro-inflammatory cytokines IL-6 and TNF-α. |
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