The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model

Qiang Fajing; Xu Xiaoyun; Li Huimin

doi:doi:10.11648/j.sr.20261405.15

Research Article |

| Peer-Reviewed

The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model

Qiang Fajing

, Xu Xiaoyun

, Li Huimin^*

Published in Science Research (Volume 14, Issue 5)

Received: 10 July 2026 Accepted: 26 August 2026 Published: 4 September 2026

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Abstract

Objective To explore the mechanism by which Chaihu Shugan Powder inhibits LPS-induced inflammation in BV2 cells based on network pharmacology, molecular docking and in vitro experiments. Method The antidepressant mechanism of Chaihu Shugan Powder was predicted by network pharmacological analysis, and the key active ingredients were screened in combination with molecular docking technology. Further construct an LPS-induced inflammatory model of BV2 cells and provide intervention treatment with Chaihu Shugan Powder. The protein levels and mRNA expression levels of TNF-α, IL-1β, IL-6 and IL-10 in the cell supernatants and intracellular tissues of each group were detected by ELISA kits and qRT-PCR. The level of NO in the cell supernatant was detected by the Greiss method; The expressions of microglial polarization markers iNOS, CD86, CD206 and Arg-1, as well as key proteins of the TNF-α/NF-κB pathway in each group of cells were detected by Western blot. Result The results of network pharmacological analysis showed that a total of 118 intersection targets were obtained. Based on the degree value > 3 (median), 35 core targets were screened out, and the traceability analysis obtained 8 key components that played a role. The results of pathway enrichment indicated that the antidepressant effect of Bupleurum evacuation might be related to signaling pathways such as TNF, PI3K-Akt, Apoptosis and MAPK. The results of the CCK-8 experiment determined that the high, medium and low administration doses of Chaihu Shugan Powder were 125, 62.5 and 31.25μg/mL, respectively. The results of the Greiss method for detecting the NO level in the cell supernatant showed that different doses of Chaihu Shugan Powder could significantly reduce the release of NO induced by LPS (P<0.001). ELISA and PCR results showed that the Chaihu Shugan Powder administration group could significantly adjust back the abnormal changes in the levels of various inflammatory factors (P<0.001, P<0.01, P<0.05). The results of Western blot detection showed that compared with the Control group, the expressions of M1-type polarization markers iNOS and CD86 in microglia of the LPS group significantly increased (P<0.001), while the expressions of M2-type polarization markers CD206 and Arg-1 significantly decreased (P<0.001). The protein contents of TNF-α, TLR4, p-IKKα/β, p-IκBα, NF-κB p65 and c-fos proteins increased (P<0.001); After treatment with Chaihu Shugan Powder, the abnormal expression of the above proteins could be significantly improved in all cases (P<0.001，P<0.01，P<0.05). The findings from molecular docking indicated that all eight essential components demonstrated strong binding affinities with the proteins previously mentioned. Conclusion Chaihu Shugan Powder can exert an antidepressant effect by inhibiting the polarization of microglia to M1 type and regulating the TNF-α/NF-κB signaling pathway, thereby suppressing the expression of inflammatory factors.

Published in	Science Research (Volume 14, Issue 5)
DOI	10.11648/j.sr.20261405.15
Page(s)	296-307
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2026. Published by Science Publishing Group

Keywords

Chaihu Shugan Powder, Lipopolysaccharide, BV2 Cells, Depression

1. 引言

抑郁症作为一种临床常见的情绪障碍类精神疾病，其发病率逐年稳步上升。抑郁症患者的临床表现通常为持续情绪低落、失眠、自我怀疑等。在病情较为严重的患者中，还可能出现自残、自杀企图等极端行为

[1]

。近年来，抑郁症的流行病学研究揭示了抑郁症在全球范围内呈现显著的增长趋势。在我国抑郁症患病率逐年上升。截至2021年，中国抑郁症患者数量已达到5310万人，与1990年相比增长了54%

[2]

，且据统计每年约有28万人自杀，其中40%为不同程度的抑郁症患者

[3]

。抑郁症作为一种心境情感障碍综合征

[4]

，其高复发率和难治性对抑郁患者身心造成严重损害，不仅导致患者生活质量急剧下降，同时也对家庭和社会造成了一定的经济负担。在当今社会，抑郁症已成为威胁人类身心健康的第二大疾病

[5]

。

中医中抑郁症归属于“郁证”，以情绪不宁、易怒易哭等为主要表现

[6]

。柴胡疏肝散出自明代张介宾的《景岳全书》，处方包括陈皮、柴胡、川芎、枳壳、芍药、甘草和香附，具有疏肝行气、活血止痛的功效

[7]

。方中柴胡调肝气、散郁结，为君药；香附疏肝解郁、理气止痛，川芎开郁行气，活血止痛，二者为臣药，助柴胡疏肝理气止痛；佐以陈皮、枳壳理气行滞，白芍、甘草养血柔肝、缓急止痛；甘草调和诸药，兼作使药

[7]

。诸药合用，主治胸肋胀满疼痛、情志抑郁或易怒、乳房胀痛为主症的肝气郁结、气滞血瘀证

[8]

。是治疗肝郁气滞证的代表方之一，在临床上广泛用于抑郁症的治疗，且已取得显著疗效

[9]

。

目前，柴胡疏肝散抗抑郁的具体分子机制尚待深入揭示。因此本研究首先借助网络药理学预测柴胡疏肝散可能的抗抑郁机制，随后通过LPS诱导BV2小胶质细胞体外建立抑郁模型对柴胡疏肝散抗抑郁作用机制进行验证。研究结果有望为柴胡疏肝散治疗抑郁症提供新型靶点与理论依据。

2．材料与仪器

2.1．细胞

小鼠小胶质细胞（BV2）购自上海佰利莱生物科技有限公司。

2.2．实验药材

柴胡疏肝散：柴胡、白芍、陈皮、香附、川芎、甘草、枳壳均由榆林市星元医院提供。

2.3．试剂

胎牛血清（FBS）（美国Gibco公司，货号10270-106）；高糖培养基（DMEM）、青霉素-链霉素溶液、胰蛋白酶（大连美伦生物技术有限公司，货号MA0212-1、MA0348、MA0234-1；cck-8试剂盒、RIPA细胞裂解液（碧云天生物技术有限公司，货号C0038、P0013B）；DMSO（中国aladdin 公司，货号 D103272）；脂多糖（LPS）（Sigma公司，货号：L2880）；兔抗小鼠CD206、CD86、Arg-1、iNOS、TNF-α、TLR4、IKKα/β、p-IKKα/β、IκBα、p-IκBα、NF-κB p65、p-NF-κB p65和c-fos，二抗山羊抗兔IgG/HR（碧云天生物技术有限公司，货号：AF7500、 AF1447、AG8128、AF7281、AF8208、AF8187、AF0198、AF5839、AG2737、AF5851、AF5243、AF5875、AF6489）；β-Actin抗体(武汉爱博泰克生物科技有限公司，货号AC026)。

2.4．仪器

硝酸纤维素膜（NC膜）（北京博奥拓达科技有限公司）、DYY-6D电泳仪、垂直电泳转印槽（北京市六一仪器厂）、CX31型荧光倒置显微镜（日本Olympus公司）、C3000系列凝胶成像及分析系统(上海天能科技有限公司) 等。

3．方法

3.1．基于网络药理学预测柴胡疏肝散抗抑郁作用机制

3.1.1．柴胡疏肝散活性成分及相关靶点筛选

通过TCMSP数据库（https://tcmsp-e.com/tcmsp. php）筛选柴胡疏肝散药物活性成分，以柴胡疏肝散组方药物柴胡、陈皮、川芎、香附、枳壳、白芍、甘草为检索词，筛选条件设定为口服生物利用度（OB）≥30%且类药性（DL）≥0.18。通过TCMSP数据库和SwissTargetPrediction数据库获取上述活性成分靶点，并将各成分的靶点信息进行汇总去重，得到柴胡疏肝散药物靶点。

3.1.2．抑郁症疾病靶点获取

以“depression”为检索词，在GeneCards (https://www.genecards.org)和OMIM (https://www.omim.org/)数据库检索抑郁症相关作用靶点，去重后，得到抑郁症疾病靶点。

3.1.3．蛋白相互作用网络构建

借助Venny2.1.0平台（https://bioinfogp.cnb. csic. es/ tools/venny），对药物靶点与疾病靶点进行交集分析，获得共同靶点。将交集靶点提交至STRING（https://string-db. org）数据库，物种参数设定为“Homo sapiens”，置信度阈值设为≥0.9，剔除无关联节点后构建蛋白互作（PPI）网络，将构建的PPI网络导入Cytoscape3.9.1软件中进行拓扑分析，计算degree值，将degree值大于中位数的靶点作为柴胡疏肝散治疗抑郁症的核心靶点。

3.1.4．药物-活性成分-靶点网络构建

将构建PPI网络分析得到的核心靶点溯源其对应化学成分与中药，导入Cytoscape3.9.1软件，构建药物-活性成分-核心靶点网络，并进行拓扑分析，得到柴胡疏肝散治疗抑郁症的主要活性成分。

3.1.5．GO和KEGG通路富集分析

将PPI网络分析中删去无关联靶点剩余的靶点导入DAVID（https://david. ncifcrf.gov/）数据库中，进行GO和KEGG通路富集分析，并利用微生信在线平台（http://bioinformatics.com.cn）对富集结果进行可视化。

3.2．基于BV2细胞体外模型实验验证

3.2.1．BV2细胞复苏与培养

从液氮中取出细胞，立即放入37 ℃水浴中，缓缓晃动冻存管至冻存液完全溶解；随后将细胞移入含5 mL培养基的离心管，室温下1000 rpm离心5 min，弃去上清液，用1 mL新鲜培养基重悬细胞，接种于含DMEM完全培养基的培养皿中，在37 ℃、5% CO2条件下培养。待细胞密度达到80%时进行传代：用移液器轻轻吹打皿底使贴壁细胞脱落，收集全部培养液至15 mL离心管中，室温1000 rpm离心5 min，弃上清；加入PBS洗涤一次，再次于室温下1000 rpm离心5 min，去除上清液；加入完全培养基吹打分散细胞，制成单细胞悬液，按1:3比例传代，随后放入细胞培养箱中继续培养。

3.2.2．柴胡疏肝散水提液的制备

将按照一定比例称取柴胡疏肝散复方中各味药并加入10倍量水浸泡30 min，随后加热回流提取两次，每次1.5 h，合并两次滤液，浓缩，并用0.22 μm微孔滤膜过滤除菌后无菌分装存放在-20℃条件下保存。

3.2.3．CCK-8实验筛选柴胡疏肝散给药浓度

取处于对数生长期、生长状态良好的BV2细胞，进行计数，以5×10³个/孔，接入96孔板设置空白组，于37℃、5%CO₂条件下培养24h；待细胞完全贴壁后进行给药处理，根据预实验结果，设置柴胡疏肝散浓度梯度为4000、2000、1000、500、250、125、62.5和31.25μg/mL，于37 ℃、5% CO₂培养箱中培养，处理24 h后，每孔加入10 μL CCK-8试剂，培养箱中培养2 h后，使用酶标仪在450 nm处检测每孔的吸光值。实验重复3次。计算公式：细胞存活率=[(实验孔吸光度)-(空白孔吸光度)]/[(对照孔吸光度)-(空白孔吸光度)]*100%。

3.2.4．BV2细胞分组及给药

实验设置5个组别：正常对照组、模型组，以及柴胡疏肝散低、中、高剂量组。除正常对照组外，其余各组均以1 μg·mL^-1的LPS处理4小时，用以构建体外抑郁模型。

3.2.5．Greiss法检测细胞上清液中NO水平

细胞分组和给药按“2.2.4”项下进行，给药后分别收集每组细胞培养上清液，按照相应试剂盒说明书，以Greiss法检测NO水平。

3.2.6．ELISA试剂盒法检测各组细胞中各细胞因子的蛋白表达量

参照“2.2.4”项所述方法完成分组。将BV2细胞按1×10⁵/mL的密度接种于6孔板中，经不同浓度药物处理24 h后，分别收集各组细胞上清液，并对其炎症因子蛋白表达水平进行检测。

3.2.7．qRT-PCR法检测各组细胞中各细胞因子的mRNA表达量

实验分组按照“2.2.4”项下进行。将BV2细胞按1×10⁵/mL的密度接种于6孔板中，用不同浓度药物培养细胞24 h后，使用RNA提取液Trizol提取各组细胞总的RNA，检测RNA浓度及纯度；将提取的RNA 逆转录为cDNA，以引物cDNA为模板，使用RT（q）-PCR检测试剂盒进行PCR扩增，以β-actin为内参，目的基因相对丰度通过2^–ΔΔCt法计算得出。基因引物序列信息见表1。

表1 引物列表。

基因	引物序列（5^，→3^，）
IL-6	gccttcttgggactgatgct
IL-6	agcctccgacttgtgaagtg
TNF-α	atggcctccctctcatcagt
TNF-α	aaggtacaacccatcggctg
IL-1β	gggctgcttccaaacctttg
IL-1β	aagacacaggtagctgccac
IL-10	cagagaagcatggcccagaa
IL-10	gctccactgccttgctctta
β-actin	tactgctctggctcctagca
β-actin	cggactcatcgtactcctgc

3.2.8．Western blot法测定各组细胞内小胶质细胞极化相关蛋白表达水平

按“2.2.4”节分组培养结束后，收集细胞并加入RIPA裂解液提取总蛋白，采用BCA法测定蛋白浓度。上样量经归一化处理后，通过SDS-PAGE电泳分离，电转移至膜上，依次完成特异性抗体孵育、显色及曝光。最后利用Image J软件对各条带的相对灰度值进行定量分析。

3.2.9．Western blot法测定各组细胞内TNF-α/NF-κB信号通路蛋白表达水平

测定方法同“2.2.8”项下。

3.2.10．统计方法

实验数据均用Graphpad Prism 9.5软件进行分析整理，两两组间比较用t检验，多组间比较采用单因素方差分析，P<0.05为具有统计学意义。

3.3．分子对接验证

将药物-活性成分-核心靶点网络中筛选degree值>15的活性成分，并获取PPI网络中TNF/NF-κB信号通路相关蛋白，分别通过PubChem（https://pubchem.ncbi.nlm.nih.gov）数据库和PDB（https://www.rcsb.org）数据库下载3D结构，导入AutoDock1.5.7软件，进行除水、加氢等处理后，使用Vina脚本进行分子对接。最后，通过PyMOL软件对对接结果进行可视化呈现。

4．结果

4.1．网络药理学分析结果

4.1.1．柴胡疏肝散抗抑郁相关活性成分及潜在靶点

运用TCMSP数据库对柴胡疏肝散中各组成药物的化学成分进行检索，共得到138个化学成分，并对应119个药物作用靶点；通过GeneCards数据库得到抑郁症疾病靶点共17110个；随后将药物靶点与疾病靶点进行交集，得到118个交集靶点（图1），作为柴胡疏肝散治疗抑郁症的作用。

Download: Download full-size image

Figure 1. 图1 药物和疾病交集靶点Venny图。

4.1.2．蛋白相互作用网络分析

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Figure 2. 图2 118个交集靶点PPI网络图。

将118个交集靶点导入STRING数据库中，构建PPI网络图（图2）。进一步通过Cytoscape3.9.1软件对PPI网络进行分析，计算degree值，degree值>3（中位数）的靶点共35个确定为柴胡疏肝散治疗抑郁症的核心靶点（图3），通过核心靶点溯源其对应化学成分及中药，绘制“中药-化学成分-核心靶点”网络图，对网络的degree值进行计算，初步确定degree值>15的化学成分（槲皮素、山柰酚、异鼠李素、木犀草素、柚皮素、川陈皮素、β-谷甾醇、甘草查尔酮）为发挥作用的关键成分（图4）。

Download: Download full-size image

Figure 3. 图3 35个核心靶点PPI网络图。

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Figure 4. 图4 中药-化学成分-核心靶点网络图。

4.1.3．GO和KEGG通路富集分析结果

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Figure 5. 图5 GO和KEGG通路富集结果图（左：GO富集结果；右：KEGG富集结果）。

随后将118个柴胡疏肝散抗抑郁潜在靶点导入DAVID数据库进行通路富集分析。GO富集分析显示，共涉及生物过程（BP）条目179个、细胞组分（CC）条目60个、分子功能（MF）条目153个，按count数排序筛选条目并绘制柱状图（图5，左）。BP主要涉及RNA聚合酶II正调控转录、基因表达的正调控、DNA模板转录的正调控、凋亡过程负向调控等，CC主要涉及胞质、细胞核、细胞质、核浆等，MF主要涉及酶结合、相同的蛋白质结合、核受体活性、蛋白结合等。

潜在靶点KEGG通路富集分析共获得信号通路124条，根据各通路富集基因数目排序并选取前30条信号通路进行可视化（图5，右）。主要包括TNF信号通路、PI3K-Akt信号通路、Apoptosis信号通路、MAPK信号通路等。

4.2．实验验证结果

4.2.1．不同浓度柴胡疏肝散对BV2细胞存活率的影响

不同浓度的柴胡疏肝散处理BV2细胞24h后，用cck-8法测定各组细胞存活率，结果如图6所示。根据实验结果，确定柴胡疏肝散后续的高、中、低给药浓度为125、62.5和31.25μg/mL。

注：与Control组相比，^###P<0.001；^##P<0.01；^#P<0.05

Download: Download full-size image

Figure 6. 图6 柴胡疏肝散对BV2细胞存活率的影响结果。

4.2.2．柴胡疏肝散对BV2细胞上清液中NO的影响

Greiss法检测细胞上清液中NO水平，结果如图7所示，LPS诱导能显著增加BV2细胞上清液中的NO释放量（P<0.001），使BV2细胞发生炎症反应，给予不同剂量的柴胡疏肝散治疗后，能不同程度的改善细胞上清液中NO的水平，抑制LPS诱导引起的炎症反应。

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Figure 7. 图7 NO浓度测定结果。

注：与Control组相比，^###P<0.001。与LPS组相比，^***P<0.001

4.2.3．柴胡疏肝散对BV2细胞中各细胞因子变化水平的影响

通过ELISA试剂盒和PCR法检测各组细胞中炎症因子TNF-α、IL-1β、IL-10和IL-6的蛋白和mRNA变化水平，结果如图8所示。与Control组相比，LPS组TNF-α、IL-1β和IL-6细胞因子的蛋白和mRNA表达水平显著增加(P<0.001)；IL-10的含量显著降低(P<0.001);与LPS组相比，柴胡疏肝散给药组TNF-α、IL-1β、IL-6和IL-10的蛋白和mRNA表达水平均显著回调(P<0.001，P<0.01，P<0.05) 。

注：与Control组相比，^###P<0.001。与LPS组相比，^***P<0.001；^**P<0.01；^*P<0.05

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Figure 8. 图8 各组细胞及上清液中炎症因子的变化情况。

4.2.4．柴胡疏肝散对各组细胞内小胶质细胞极化相关蛋白水平变化的影响

测定各组细胞内小胶质细胞极化相关蛋白CD86、iNOS、Arg-1和CD206的蛋白含量，条带结果如图9，量化结果如图10。与Control组相比，LPS组细胞内M1型标记物CD86和iNOS蛋白表达显著增加(P<0.001)，M2型标记物Arg-1和CD206的蛋白表达显著降低(P<0.001)。与LPS组相比，柴胡疏肝散各给药组细胞内M1型标记物CD86和iNOS蛋白表达显著减少(P<0.001，P<0.01)，M2型标记物Arg-1和CD206的蛋白表达显著回调(P<0.001，P<0.01)，结果表明，柴胡疏肝散能促进LPS诱导的小胶质细胞由促炎的M1型转向抑炎的M2型。

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Figure 9. 图9 小胶质细胞极化相关蛋白条带图。

注：与Control组相比，^###P<0.001。与LPS组相比，^***P<0.001；^**P<0.01；^*P<0.05

Download: Download full-size image

Figure 10. 图10 小胶质细胞极化相关蛋白条带量化结果。

4.2.5．柴胡疏肝散对各组细胞TNF/NF-κB信号通路相关蛋白水平变化的影响

测定各组细胞内TNF-α、TLR4、p-IKKα/β、p-IKBα、NF-κB p65和c-fos蛋白含量，条带结果如图11，量化结果见图12。与Control组相比，LPS组细胞内TNF-α、TLR4、p-IKKα/β、p-IKBα、NF-κB p65和c-fos蛋白含量增加; 与LPS组相比，柴胡疏肝散给药组细胞内TNF-α、TLR4、p-IKKα/β、p-IKBα、NF-κB p65和c-fos 蛋白相对水平降低(P<0.001，P<0.01，P<0.05)。

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Figure 11. 图11 TNF/NF-κB信号通路相关蛋白条带图。

注：与Control组相比，^###P<0.001。与LPS组相比，***P<0.001；**P<0.01；*P<0.05

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Figure 12. 图12 TNF/NF-κB信号通路蛋白条带量化结果。

4.3．分子对接结果

将中药-化学成分-核心靶点网络图degree>15的活性成分与TNF/NF-κB信号通路相关蛋白（TNF-α、TLR4、IKKα/β、NF-κB p65、IKBα和c-fos）分别进行分子对接，对接结合能见图13。各成分与各蛋白对接的结合能均小于-5.0 kcal/mol，表明活性成分与靶点结合活性较好、程度稳定。结果提示，上述活性成分可能够通过调节TNF/NF-κB信号通路相关蛋白的变化发挥抗抑郁作用。在与各蛋白对接的各个化学成分中选择结合能较好的组合绘制分子对接示意图，见图14。

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Figure 13. 图13 分子对接结合能热图。

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Figure 14. 图14 分子对接示意图。

5．讨论

抑郁症作为一种复杂的精神疾病，其发病机制复杂，涉及生理因素、遗传因素、环境压力等多种因素。目前临床上对于抑郁症的治疗主要还是选取西药治疗的方式，虽然能够较好的缓解抑郁症状，但是副作用较多

[10]

，因此中药治疗抑郁症展现出较大的优势。

柴胡疏肝散作为中医中的经典方剂，在中医理论中主要用于疏肝解郁、调和气血。现代医学研究表明，抑郁症的发生与肝郁气滞等中医证型密切相关，其病理生理机制涉及神经内分泌失调、神经炎症等诸多因素

[11]

。已有的大量研究表明，柴胡疏肝散具有良好的抗抑郁作用，但对于其抗抑郁活性成分和作用机制尚未完全阐明。因此，本文通过网络药理学预测结合LPS诱导BV2小胶质细胞的抑郁模型，探究柴胡疏肝散的抗抑郁作用机制。

本研究通过网络药理学预测，筛选出柴胡疏肝散抗抑郁潜在作用靶点118个，核心靶点35个和8个关键成分（槲皮素、山柰酚、异鼠李素、木犀草素、柚皮素、川陈皮素、β-谷甾醇、甘草查尔酮）。通路富集结果显示柴胡疏肝散发挥抗抑郁作用可能与TNF信号通路、PI3K-Akt信号通路、和MAPK信号通路等信号通路相关，因此本研究进一步根据通路富集结果中的P值以及各个通路的富集基因确定了TNF-α/NF-κB信号通路作为研究对象。

LPS可诱导神经炎症，常被用作抑郁症研究的经典模型。已有的研究表明，LPS激活BV2细胞AKT信号通路，促进下游NF-κB介导的炎症介质转录，导致炎症反应，影响神经细胞的正常功能及状态

[12]

。本研究实验结果表明，经LPS诱导后，BV2细胞上清液中NO释放明显增加，同时促炎因子IL-1β、IL-6和TNF-α的表达水平亦显著上升。此外，大量释放的TNF-α可借助其相应受体激活IKK复合物，促使IκBα发生降解，进而释放NF-κB二聚体并转位进入细胞核，最终调控炎症相关基因表达

[13]

。这种机制可以进一步增强TLR4信号通路的激活，形成正反馈环路。而NF-κB是一种由p50和p65亚基组成的异源二聚体核转录因子，在炎症反应和免疫调节中起重要作用

[14]

。在静息状态下，NF-κB与其抑制蛋白IκBα结合，以无活性形式存在于细胞质中

[15]

。当受到应激、炎症或氧化应激等刺激时，IκBα被磷酸化并降解，释放出NF-κB并使其易位至细胞核，进而启动下游炎症相关基因的转录

[16]

。研究表明，在抑郁症患者脑区，NF-κB被异常激活，激活其下游相关蛋白，并导致其下游炎症相关基因表达显著升高，IL-6、TNF-α等促炎因子大量产生

[17]

。在抑郁症的神经炎症微环境中，当TNF-α/NF-κB通路激活后，诱导大量炎症因子的产生，进一步促进了小胶质细胞向M1促炎表型极化，使iNOS和CD86 的表达显著增加；相反，激活的M1型细胞持续释放的TNF-α又可通过自分泌或旁分泌进一步激活邻近细胞的NF-κB，形成正反馈通路进而放大炎症反应

[18]

。

小胶质细胞是CNS先天免疫系统的第一线，积极调节健康和无序大脑的微环境变化。小胶质细胞激活调节炎症、突触细化、突触修剪和神经元连接

[19]

。抑郁症被认为是一种小胶质细胞相关疾病（小胶质细胞病）

[20]

。小胶质细胞的活化被认为是神经炎症的具体表现，是各种刺激诱导的神经炎症反应的关键聚合，也是促炎因子和氧化应激的重要来源

[21]

。大量证据表明，小胶质细胞介导的神经炎症与抑郁症的发生发展相关

[22, 23]

，临床中一些常用的抗抑郁药也会影响小胶质细胞的激活和神经炎症的变化情况从而发挥一定的抗抑郁作用

[24-26]

。

小胶质细胞根据不同的刺激因子分为促炎的M1表型和抗炎的M2表型

[27]

，M1表型由LPS和/或IFN-γ刺激诱导，促使M1表型标记物CD32、CD86、iNOS等表达升高，并且M1型小胶质细胞大量分泌促炎因子、趋化因子、环氧化酶-2、活性氧等；M2表型是由IL-4/IL-13刺激诱导，IL-4能够与其受体结合从而激活STAT6，使小胶质细胞转变为抗炎表型，增加Arg-1、CD206、甘露糖受体等的表达，并释放一系列抗炎因子如IL-4、IL-10、IL-13、IL-1RA等

[28-30]

。已有研究表明，在LPS诱导的抑郁小鼠海马组织中的小胶质细胞为促炎的M1表型，进而促进炎症因子大量释放，加重神经炎症

[31, 32]

。给予一定的药物治疗后促进小胶质细胞向M2表型转化，促使小胶质细胞分泌抗炎因子，从而发挥抗抑郁作用[31, 33]。本实验结果也证实，经LPS诱导后，能够激活TNF-α/NF-κB信号通路，并且增加M1型标记物iNOS和CD86 的表达。给予柴胡疏肝散治疗后显著降低了促炎因子的表达，抑制了TNF-α/NF-κB信号通路的激活和小胶质细胞向M1表型极化，促进其向M2表型极化。

最后，为考察8种关键活性成分（槲皮素、山柰酚、异鼠李素、木犀草素、柚皮素、川陈皮素、β-谷甾醇及甘草查尔酮）与TNF-α/NF-κB信号通路中TNF-α、TLR4、IKKα/β、NF-κB p65、IKBα和c-fos等蛋白的相互作用，本研究进一步开展了分子对接实验。结果显示，上述成分成分与各靶点蛋白均具有良好的结合能。由此推测，上述关键成分可能通过调控TNF-α/NF-κB通路发挥抗抑郁作用，该机制仍需后续实验加以证实。

综上，柴胡疏肝散可诱导小胶质细胞由M1型向M2表型转化，抑制TNF-α/NF-κB信号通路，从而下调炎症因子表达，实现抗抑郁效应。该结果为柴胡疏肝散的临床运用奠定了理论基础，但其具体机制仍需深入研究。后续研究应加强体内实验验证，解析其多靶点、多通路协同调控网络，并评估临床应用中的安全性与有效性。

基金项目

陕西省科协青年人才托举计划项目（20240317）。

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Fajing, Q., Xiaoyun, X., Huimin, L. (2026). The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model. Science Research, 14(5), 296-307. https://doi.org/10.11648/j.sr.20261405.15

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ACS Style

Fajing, Q.; Xiaoyun, X.; Huimin, L. The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model. Sci. Res. 2026, 14(5), 296-307. doi: 10.11648/j.sr.20261405.15

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AMA Style

Fajing Q, Xiaoyun X, Huimin L. The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model. Sci Res. 2026;14(5):296-307. doi: 10.11648/j.sr.20261405.15

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@article{10.11648/j.sr.20261405.15,
  author = {Qiang Fajing and Xu Xiaoyun and Li Huimin},
  title = {The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model},
  journal = {Science Research},
  volume = {14},
  number = {5},
  pages = {296-307},
  doi = {10.11648/j.sr.20261405.15},
  url = {https://doi.org/10.11648/j.sr.20261405.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sr.20261405.15},
  abstract = {Objective To explore the mechanism by which Chaihu Shugan Powder inhibits LPS-induced inflammation in BV2 cells based on network pharmacology, molecular docking and in vitro experiments. Method The antidepressant mechanism of Chaihu Shugan Powder was predicted by network pharmacological analysis, and the key active ingredients were screened in combination with molecular docking technology. Further construct an LPS-induced inflammatory model of BV2 cells and provide intervention treatment with Chaihu Shugan Powder. The protein levels and mRNA expression levels of TNF-α, IL-1β, IL-6 and IL-10 in the cell supernatants and intracellular tissues of each group were detected by ELISA kits and qRT-PCR. The level of NO in the cell supernatant was detected by the Greiss method; The expressions of microglial polarization markers iNOS, CD86, CD206 and Arg-1, as well as key proteins of the TNF-α/NF-κB pathway in each group of cells were detected by Western blot. Result The results of network pharmacological analysis showed that a total of 118 intersection targets were obtained. Based on the degree value > 3 (median), 35 core targets were screened out, and the traceability analysis obtained 8 key components that played a role. The results of pathway enrichment indicated that the antidepressant effect of Bupleurum evacuation might be related to signaling pathways such as TNF, PI3K-Akt, Apoptosis and MAPK. The results of the CCK-8 experiment determined that the high, medium and low administration doses of Chaihu Shugan Powder were 125, 62.5 and 31.25μg/mL, respectively. The results of the Greiss method for detecting the NO level in the cell supernatant showed that different doses of Chaihu Shugan Powder could significantly reduce the release of NO induced by LPS (PPPPPPPPPPConclusion Chaihu Shugan Powder can exert an antidepressant effect by inhibiting the polarization of microglia to M1 type and regulating the TNF-α/NF-κB signaling pathway, thereby suppressing the expression of inflammatory factors.},
 year = {2026}
}

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TY  - JOUR
T1  - The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model
AU  - Qiang Fajing
AU  - Xu Xiaoyun
AU  - Li Huimin
Y1  - 2026/09/04
PY  - 2026
N1  - https://doi.org/10.11648/j.sr.20261405.15
DO  - 10.11648/j.sr.20261405.15
T2  - Science Research
JF  - Science Research
JO  - Science Research
SP  - 296
EP  - 307
PB  - Science Publishing Group
SN  - 2329-0927
UR  - https://doi.org/10.11648/j.sr.20261405.15
AB  - Objective To explore the mechanism by which Chaihu Shugan Powder inhibits LPS-induced inflammation in BV2 cells based on network pharmacology, molecular docking and in vitro experiments. Method The antidepressant mechanism of Chaihu Shugan Powder was predicted by network pharmacological analysis, and the key active ingredients were screened in combination with molecular docking technology. Further construct an LPS-induced inflammatory model of BV2 cells and provide intervention treatment with Chaihu Shugan Powder. The protein levels and mRNA expression levels of TNF-α, IL-1β, IL-6 and IL-10 in the cell supernatants and intracellular tissues of each group were detected by ELISA kits and qRT-PCR. The level of NO in the cell supernatant was detected by the Greiss method; The expressions of microglial polarization markers iNOS, CD86, CD206 and Arg-1, as well as key proteins of the TNF-α/NF-κB pathway in each group of cells were detected by Western blot. Result The results of network pharmacological analysis showed that a total of 118 intersection targets were obtained. Based on the degree value > 3 (median), 35 core targets were screened out, and the traceability analysis obtained 8 key components that played a role. The results of pathway enrichment indicated that the antidepressant effect of Bupleurum evacuation might be related to signaling pathways such as TNF, PI3K-Akt, Apoptosis and MAPK. The results of the CCK-8 experiment determined that the high, medium and low administration doses of Chaihu Shugan Powder were 125, 62.5 and 31.25μg/mL, respectively. The results of the Greiss method for detecting the NO level in the cell supernatant showed that different doses of Chaihu Shugan Powder could significantly reduce the release of NO induced by LPS (PPPPPPPPPPConclusion Chaihu Shugan Powder can exert an antidepressant effect by inhibiting the polarization of microglia to M1 type and regulating the TNF-α/NF-κB signaling pathway, thereby suppressing the expression of inflammatory factors.
VL  - 14
IS  - 5
ER  -

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Author Information

Qiang Fajing

Clinical Pharmacy Department, Yulin Xingyuan Hospital, Yulin, China

Contact Email

http://orcid.org/0009-0002-2140-7216
Xu Xiaoyun

Clinical Pharmacy Department, Yulin Xingyuan Hospital, Yulin, China

http://orcid.org/0009-0003-3544-4429
Li Huimin

Clinical Pharmacy Department, Yulin Xingyuan Hospital, Yulin, China;Science and Education Department, Yulin Hospital, the First Affiliated Hospital of Xi'an Jiaotong University, Yulin, China

Contact Email

http://orcid.org/0000-0001-9598-5698

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Abstract
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1. 1. 引言
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2．材料与仪器
3．方法
4．结果
5．讨论
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Figure 1

Figure 1. 图 1 药物和疾病交集靶点Venny图。
Figure 2

Figure 2. 图 2 118个交集靶点PPI网络图。
Figure 3

Figure 3. 图 3 35个核心靶点PPI网络图。
Figure 4

Figure 4. 图 4 中药-化学成分-核心靶点网络图。
Figure 5

Figure 5. 图 5 GO和KEGG通路富集结果图（左：GO富集结果；右：KEGG富集结果）。
Figure 6

Figure 6. 图 6 柴胡疏肝散对BV2细胞存活率的影响结果。
Figure 7

Figure 7. 图 7 NO浓度测定结果。
Figure 8

Figure 8. 图 8 各组细胞及上清液中炎症因子的变化情况。
Figure 9

Figure 9. 图 9 小胶质细胞极化相关蛋白条带图。
Figure 10

Figure 10. 图 10 小胶质细胞极化相关蛋白条带量化结果。
Figure 11

Figure 11. 图 11 TNF/NF-κB信号通路相关蛋白条带图。
Figure 12

Figure 12. 图 12 TNF/NF-κB信号通路蛋白条带量化结果。
Figure 13

Figure 13. 图 13 分子对接结合能热图。
Figure 14

Figure 14. 图 14 分子对接示意图。

Table 1

表1 引物列表。

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APA Style

Fajing, Q., Xiaoyun, X., Huimin, L. (2026). The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model. Science Research, 14(5), 296-307. https://doi.org/10.11648/j.sr.20261405.15

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ACS Style

Fajing, Q.; Xiaoyun, X.; Huimin, L. The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model. Sci. Res. 2026, 14(5), 296-307. doi: 10.11648/j.sr.20261405.15

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AMA Style

Fajing Q, Xiaoyun X, Huimin L. The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model. Sci Res. 2026;14(5):296-307. doi: 10.11648/j.sr.20261405.15

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@article{10.11648/j.sr.20261405.15,
  author = {Qiang Fajing and Xu Xiaoyun and Li Huimin},
  title = {The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model},
  journal = {Science Research},
  volume = {14},
  number = {5},
  pages = {296-307},
  doi = {10.11648/j.sr.20261405.15},
  url = {https://doi.org/10.11648/j.sr.20261405.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sr.20261405.15},
  abstract = {Objective To explore the mechanism by which Chaihu Shugan Powder inhibits LPS-induced inflammation in BV2 cells based on network pharmacology, molecular docking and in vitro experiments. Method The antidepressant mechanism of Chaihu Shugan Powder was predicted by network pharmacological analysis, and the key active ingredients were screened in combination with molecular docking technology. Further construct an LPS-induced inflammatory model of BV2 cells and provide intervention treatment with Chaihu Shugan Powder. The protein levels and mRNA expression levels of TNF-α, IL-1β, IL-6 and IL-10 in the cell supernatants and intracellular tissues of each group were detected by ELISA kits and qRT-PCR. The level of NO in the cell supernatant was detected by the Greiss method; The expressions of microglial polarization markers iNOS, CD86, CD206 and Arg-1, as well as key proteins of the TNF-α/NF-κB pathway in each group of cells were detected by Western blot. Result The results of network pharmacological analysis showed that a total of 118 intersection targets were obtained. Based on the degree value > 3 (median), 35 core targets were screened out, and the traceability analysis obtained 8 key components that played a role. The results of pathway enrichment indicated that the antidepressant effect of Bupleurum evacuation might be related to signaling pathways such as TNF, PI3K-Akt, Apoptosis and MAPK. The results of the CCK-8 experiment determined that the high, medium and low administration doses of Chaihu Shugan Powder were 125, 62.5 and 31.25μg/mL, respectively. The results of the Greiss method for detecting the NO level in the cell supernatant showed that different doses of Chaihu Shugan Powder could significantly reduce the release of NO induced by LPS (PPPPPPPPPPConclusion Chaihu Shugan Powder can exert an antidepressant effect by inhibiting the polarization of microglia to M1 type and regulating the TNF-α/NF-κB signaling pathway, thereby suppressing the expression of inflammatory factors.},
 year = {2026}
}

Copy | Download

TY  - JOUR
T1  - The Effect of Chaihu Shugan Powder on Neuroinflammation in Depression Was Explored Based on the LPS-induced BV2 Inflammatory Cell Model
AU  - Qiang Fajing
AU  - Xu Xiaoyun
AU  - Li Huimin
Y1  - 2026/09/04
PY  - 2026
N1  - https://doi.org/10.11648/j.sr.20261405.15
DO  - 10.11648/j.sr.20261405.15
T2  - Science Research
JF  - Science Research
JO  - Science Research
SP  - 296
EP  - 307
PB  - Science Publishing Group
SN  - 2329-0927
UR  - https://doi.org/10.11648/j.sr.20261405.15
AB  - Objective To explore the mechanism by which Chaihu Shugan Powder inhibits LPS-induced inflammation in BV2 cells based on network pharmacology, molecular docking and in vitro experiments. Method The antidepressant mechanism of Chaihu Shugan Powder was predicted by network pharmacological analysis, and the key active ingredients were screened in combination with molecular docking technology. Further construct an LPS-induced inflammatory model of BV2 cells and provide intervention treatment with Chaihu Shugan Powder. The protein levels and mRNA expression levels of TNF-α, IL-1β, IL-6 and IL-10 in the cell supernatants and intracellular tissues of each group were detected by ELISA kits and qRT-PCR. The level of NO in the cell supernatant was detected by the Greiss method; The expressions of microglial polarization markers iNOS, CD86, CD206 and Arg-1, as well as key proteins of the TNF-α/NF-κB pathway in each group of cells were detected by Western blot. Result The results of network pharmacological analysis showed that a total of 118 intersection targets were obtained. Based on the degree value > 3 (median), 35 core targets were screened out, and the traceability analysis obtained 8 key components that played a role. The results of pathway enrichment indicated that the antidepressant effect of Bupleurum evacuation might be related to signaling pathways such as TNF, PI3K-Akt, Apoptosis and MAPK. The results of the CCK-8 experiment determined that the high, medium and low administration doses of Chaihu Shugan Powder were 125, 62.5 and 31.25μg/mL, respectively. The results of the Greiss method for detecting the NO level in the cell supernatant showed that different doses of Chaihu Shugan Powder could significantly reduce the release of NO induced by LPS (PPPPPPPPPPConclusion Chaihu Shugan Powder can exert an antidepressant effect by inhibiting the polarization of microglia to M1 type and regulating the TNF-α/NF-κB signaling pathway, thereby suppressing the expression of inflammatory factors.
VL  - 14
IS  - 5
ER  -

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