Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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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Ma Tengteng, Yang Jianyu, Yuan Yun, Luo Haiyun, Wei Yubin, Meng Jingyuan, Wang Xingping, Xie Jianping, Guo Ying
Аннотация
OBJECTIVES: 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.
CONCLUSIONS: 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.
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.
CONCLUSIONS: 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.