四氢姜黄素通过调控SIRT1/NF-κB通路改善神经炎症与神经营养平衡缓解慢性束缚应激小鼠的抑郁样行为

doi:10.12122/j.issn.1673-4254.2026.08.01

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (8): 1719-1729.doi: 10.12122/j.issn.1673-4254.2026.08.01

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四氢姜黄素通过调控SIRT1/NF-κB通路改善神经炎症与神经营养平衡缓解慢性束缚应激小鼠的抑郁样行为

马滕滕¹(), 杨建宇¹(), 袁云¹, 罗海芸¹, 魏玉彬¹, 孟靖源¹, 王兴坪¹, 谢建平²(), 郭英¹()

^1.昆明医科大学基础医学院药理学系，云南昆明 650500
^2.云南民族大学图书馆技术服务部，云南昆明 650500

收稿日期:2026-01-05 接受日期:2026-05-13 出版日期:2026-08-20 发布日期:2026-08-01
通讯作者: 谢建平,郭英 E-mail:2390484784@qq.com;yangjianyu@kmmu.edu.cn;26328188@qq.com;guoying@kmmu.edu.cn
作者简介:马滕滕，硕士，E-mail：2390484784@qq.com
杨建宇，硕士，副教授，E-mail：yangjianyu@kmmu.edu.cn

Tetrahydrocurcumin ameliorates depression-like behaviors in chronic restraint stress mice by modulating neuroinflammation and neurotrophic balance via the SIRT1/NF-κB pathway

Tengteng MA¹(), Jianyu YANG¹(), Yun YUAN¹, Haiyun LUO¹, Yubin WEI¹, Jingyuan MENG¹, Xingping WANG¹, Jianping XIE²(), Ying GUO¹()

^1.Department of Pharmacology, Faculty of Basic Medical Science, Kunming Medical University, Kunming 650500, China
^2.Department of Technical Service, Library of Yunnan Minzu University, Kunming 650500, China

Received:2026-01-05 Accepted:2026-05-13 Online:2026-08-20 Published:2026-08-01
Contact: Jianping XIE, Ying GUO E-mail:2390484784@qq.com;yangjianyu@kmmu.edu.cn;26328188@qq.com;guoying@kmmu.edu.cn
About author:First author contact:（马滕滕、杨建宇并列第一作者）
Supported by:
National Natural Science Foundation of China(82060650);国家自然科学基金(82060650);Yunnan Provincial Program for Talents Reserve of Young and Middle-aged Academic and Technical Leaders(202405AC350045);云南省中青年学术和技术带头人后备人才项目(202405AC350045)

摘要/Abstract

摘要：

目的探讨四氢姜黄素（THC）是否通过调控SIRT1/NF-κB通路改善神经炎症和神经营养平衡，从而缓解小鼠抑郁样行为。方法采用慢性束缚应激（CRS）建立小鼠抑郁模型。小鼠接受THC（2.5、5、10 mg·kg^-1·d^-1）或舍曲林（10 mg·kg^-1·d^-1）治疗21 d。通过旷场实验、高架十字迷宫、悬尾实验和强迫游泳实验评小鼠估焦虑和抑郁样行为。采用ELISA、Western blotting和免疫组化检测小鼠血清和海马组织中SIRT1、p-NF-κB/NF-κB、炎症因子（TNF-α、iNOS）和神经营养因子（BDNF、GDNF、TGF-β1）水平。通过免疫荧光分析海马CA3区小胶质细胞激活标志物（Iba1）和SIRT1表达。体外实验中，使用脂多糖（LPS）刺激BV2小胶质细胞，THC单独或联合SIRT1抑制剂EX-527对细胞进行预处理，以验证通路机制。结果 THC治疗显著缓解了CRS诱导的小鼠焦虑和抑郁样行为，促进小鼠体质量增长。THC降低了CRS小鼠血清和海马中TNF-α与iNOS水平，同时提升SIRT1、BDNF、GDNF和TGF-β1表达。THC抑制了CRS小鼠海马组织中NF-κB活化，减少海马CA3区中Iba1的表达和 Iba1⁺/SIRT1⁺细胞比例，增加SIRT1表达。体外实验显示，THC减轻LPS诱导的BV2细胞NF-κB活化，降低TNF-α和iNOS表达，促进SIRT1、BDNF、GDNF和TGF-β1表达，这些效应可被EX-527有效阻断。结论 THC在CRS小鼠中发挥显著的抗抑郁样作用，其机制可能是通过激活SIRT1以抑制NF-κB介导的神经炎症并恢复神经营养因子表达，提示SIRT1/NF-κB通路是THC发挥抗抑郁作用的关键机制。

关键词: 抑郁症, 慢性束缚应激, 四氢姜黄素, 沉默信息调节因子1, 核因子κB, 神经炎症, 神经营养

Abstract:

Objective To investigate whether tetrahydrocurcumin (THC) ameliorates depression-like behaviors in mice by modulating neuroinflammation and neurotrophic balance via the SIRT1/NF‑κB pathway. Methods A mouse model of depression was established using chronic restraint stress (CRS). The mice were treated with THC (2.5, 5, or 10 mg/k) or sertraline (10 mg/kg) on a daily basis for 21 consecutive days. Anxiety- and depression-like behaviors of the mice were assessed using open field, elevated plus maze, tail suspension, and forced swimming tests. Serum levels and hippocampal expression levels of SIRT1, p-NF-κB/NF-κB, inflammatory factors (TNF-α and iNOS), and neurotrophic factors (BDNF, GDNF, and TGF-β1) were measured using ELISA, Western blotting, or immunohistochemistry. The expression levels of hippocampal CA3 microglial activation marker (Iba1) and silent information regulator 1 (SIRT1) were analyzed using immunofluorescence staining. In the in vitro experiment, BV2 microglial cells were stimulated with lipopolysaccharide (LPS) and treated with THC with or without the SIRT1 inhibitor EX-527 for validating the pathway mediating the effect of THC. Results THC treatment significantly alleviated CRS-induced anxiety- and depression-like behaviors and increased body weight gain of the mice. THC obviously reduced serum and hippocampal levels of TNF-α and iNOS, increased the expression levels of SIRT1, BDNF, GDNF, and TGF-β1, and inhibited NF‑κB activation in the hippocampus. The THC-treated mice showed significantly reduced Iba1 expression and Iba1⁺/SIRT1⁺ cells and increased SIRT1 expression in the hippocampal CA3 region. In cultured BV2 cells, THC effectively attenuated LPS-induced NF-κB activation, lowered expressions of TNF-α and iNOS, and promoted SIRT1, BDNF, GDNF, and TGF-β1 expressions; these effects were obviously blocked by treatment with EX-527, confirming SIRT1 dependence of the effect of THC. Conclusion THC produces significant antidepressant-like effects in CRS mice likely by activating SIRT1 to suppress NF‑κB-mediated neuroinflammation and restore neurotrophic factor expressions. These findings highlight the SIRT1/NF-κB pathway as a key mechanism mediating the therapeutic effect of THC against depression.

Key words: depression, chronic restraint stress, tetrahydrocurcumin, silent information regulator 1, nuclear factor kappa-B, neuroinflammation, neurotrophy

马滕滕, 杨建宇, 袁云, 罗海芸, 魏玉彬, 孟靖源, 王兴坪, 谢建平, 郭英. 四氢姜黄素通过调控SIRT1/NF-κB通路改善神经炎症与神经营养平衡缓解慢性束缚应激小鼠的抑郁样行为[J]. 南方医科大学学报, 2026, 46(8): 1719-1729.

Tengteng MA, Jianyu YANG, Yun YUAN, Haiyun LUO, Yubin WEI, Jingyuan MENG, Xingping WANG, Jianping XIE, Ying GUO. Tetrahydrocurcumin ameliorates depression-like behaviors in chronic restraint stress mice by modulating neuroinflammation and neurotrophic balance via the SIRT1/NF-κB pathway[J]. Journal of Southern Medical University, 2026, 46(8): 1719-1729.

图/表 6

Fig.1 Effects of tetrahydrocurcumin (THC) on depression-like behaviors in mice with chronic restraint stress (CRS). A: Flowchart of the experiment protocol. B: Trajectory diagram of the mice in open field test (OFT). C: Trajectory diagram of the mice in elevated plus maze (EPM) test. D: Total distance traveled of the mice in OFT. E: Percentage of distance traveled in center in OFT. F: Percentage of time in the center in OFT. G: Percentage of distance in the center in EPM test. H: Percentage of time in the center in EPM test. I: Percentage of immobility time in tail suspension test. J: Percentage of immobility time in forced swimming test. K: Growth rate of body mass. Data are presented as Mean±SE (n=10). *P<0.05, **P<0.01 vs control; #P<0.05, ##P<0.01 vs CRS.

Fig.2 Serum levels of SIRT1, TNF-α, iNOS, BDNF, GDNF and TGF-β1 in CRS mice receiving treatment with low, medium, and high doses of THC (THC-L, THC-M and THC-H groups, respectively). A: Serum levels of SIRT1. B: Serum levels of TNF-α. C: Serum levels of iNOS. D: Serum levels of BDNF. E: Serum levels of GDNF. F: Serum levels of TGF-β1. Data are presented as Mean±SE (n=4). **P<0.01 vs control group; #P<0.05, ##P<0.01 vs CRS group.

Fig.3 Effects of different doses of THC on protein expressions of SIRT1, p-NFκB/NFκB, TNF-α, iNOS, BDNF, GDNF and TGF-β1 in the hippocampus of CRS mice detected by Western blotting. A-G: Western blotting for detecting the expression levels of SIRT1, p-NFκB/NFκB, TNF-α, iNOS, BDNF and GDNF. H-I: Western blotting for detecting the expression levels of TGF-β1. Data are presented as Mean±SE (n=4). **P<0.01 vs control group; #P<0.05, ##P<0.01 vs CRS group.

Fig.4 Effects of THC on protein expressions of SIRT1, TNF-α, iNOS, BDNF, GDNF and TGF-β1 in the CA1, CA2, CA3, and DG regions of the hippocampus in CRS mice detected by immunohistochemical staining (Original magnification: ×400). A-E: Expression levels of SIRT1 in the CA1, CA2, CA3, and DG regions. F-J: Expression levels of TNF-α in the CA1, CA2, CA3, and DG regions. K-O: Expression levels of iNOS in the CA1, CA2, CA3, and DG regions. P-T: Expression levels of BDNF in the CA1, CA2, CA3, and DG regions. U-Y: Expression levels of GDNF in the CA1, CA2, CA3, and DG regions. Z-AD: Expression levels of TGF-β1 in the CA1, CA2, CA3, and DG regions. Data are presented as Mean±SE (n=3). **P<0.01 vs control group; ##P<0.01 vs CRS group.

Fig.5 Effects of THC on protein expressions of Iba1, SIRT1, and Iba1+/SIRT1+ in the CA3 region of the hippocampus in CRS mice detected by immunofluorescence staining (×400). A: Immunofluorescence staining images of the CA3 region for detecting expressions of Iba1, SIRT1, and Iba1+/SIRT1+ in different groups. B-D: Quantitative analysis of Iba1, SIRT1, and Iba1+/SIRT1+expressions (Mean±SE, n=3). **P<0.01 vs control group; ##P<0.01 vs CRS group.

Fig.6 Effects of THC on protein expressions of SIRT1, p-NFκB/NFκB, TNF-α, iNOS, BDNF, GDNF and TGF-β1 in BV2 microgliall cells induced by LPS. A-G: Western blotting for detecting the expression levels of SIRT1, p-NFκB/NFκB, TNF-α, iNOS, BDNF and GDNF. H-I: Western blotting for detecting the expression levels of TGF-β1. J-K: Immunofluorescence staining for detecting the expression levels of TNF-α (×400). Data are presented as Mean±SE (n=3). *P<0.05, **P<0.01.

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四氢姜黄素通过调控SIRT1/NF-κB通路改善神经炎症与神经营养平衡缓解慢性束缚应激小鼠的抑郁样行为

Tetrahydrocurcumin ameliorates depression-like behaviors in chronic restraint stress mice by modulating neuroinflammation and neurotrophic balance via the SIRT1/NF-κB pathway

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