Shin Joonyoung, Kim Dong-Uk, Bae Gi-Sang, Han Ji-Ye, Lim Do-Won, Lee Young-Mi, Kim Eunjae, Kwon Eunjeong, Han Dongwoon, Kim Sungchul
Institute for Global Rare Disease Network, Professional Graduate School of Korean Medicine, Wonkwang University, Iksan 54538, Republic of Korea.
Department of Pharmacology, School of Korean Medicine, Wonkwang University, Iksan 54538, Republic of Korea.
Pharmaceuticals (Basel). 2024 Oct 21;17(10):1409. doi: 10.3390/ph17101409.
Lipopolysaccharide (LPS)-induced neuroinflammation is a well-established model for studying depression-like behavior, driven by pro-inflammatory cytokines such as TNF-α and IL-1β. Mast cells (MCs) contribute to neuroinflammation by releasing mediators that exacerbate depressive-like symptoms. This study evaluates the antidepressant-like and anti-inflammatory effects of L. inflorescence extract (CSL) in an LPS-induced neuroinflammation model.
Male C57BL/6 mice were intraperitoneally injected with CSL at doses of 10, 20, and 30 mg/kg, 30 min prior to LPS (0.83 mg/kg) administration. Depressive behaviors were assessed using the sucrose preference test (SPT), tail suspension test (TST), and forced swimming test (FST). The neutrophil-to-lymphocyte ratio (NLR) was measured to assess systemic inflammation. Cytokine levels in the prefrontal cortex (PFC) were measured, and mast cell degranulation in the lymph nodes and dura mater was analyzed histologically (approval number: WKU24-64).
CSL significantly improved depressive-like behaviors and decreased the NLR, indicating reduced systemic inflammation. CSL also significantly reduced TNF-α and IL-1β levels in the PFC. Furthermore, CSL inhibited MC degranulation in the deep cervical lymph nodes and dura mater, with the strongest effects observed at 30 mg/kg.
CSL demonstrated antidepressant-like and anti-inflammatory effects in an LPS-induced neuroinflammation model, likely through the modulation of cytokine expression and mast cell activity. These results suggest the potential of CSL as a therapeutic option for treating inflammation-related depression.
脂多糖(LPS)诱导的神经炎症是一种成熟的用于研究抑郁样行为的模型,由肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)等促炎细胞因子驱动。肥大细胞(MCs)通过释放加剧抑郁样症状的介质来促进神经炎症。本研究评估了L. inflorescence提取物(CSL)在LPS诱导的神经炎症模型中的抗抑郁样和抗炎作用。
雄性C57BL/6小鼠在给予LPS(0.83 mg/kg)前30分钟,分别腹腔注射10、20和30 mg/kg剂量的CSL。使用蔗糖偏好试验(SPT)、悬尾试验(TST)和强迫游泳试验(FST)评估抑郁行为。测量中性粒细胞与淋巴细胞比值(NLR)以评估全身炎症。测量前额叶皮质(PFC)中的细胞因子水平,并通过组织学分析淋巴结和硬脑膜中的肥大细胞脱颗粒情况(批准号:WKU24 - 64)。
CSL显著改善了抑郁样行为并降低了NLR,表明全身炎症减轻。CSL还显著降低了PFC中TNF-α和IL-1β的水平。此外,CSL抑制了颈深淋巴结和硬脑膜中的肥大细胞脱颗粒,在30 mg/kg剂量时观察到最强的效果。
CSL在LPS诱导的神经炎症模型中表现出抗抑郁样和抗炎作用,可能是通过调节细胞因子表达和肥大细胞活性实现的。这些结果表明CSL作为治疗炎症相关抑郁症的治疗选择具有潜力。