The fruit of Schisandrachinensis, a plant widely used in traditional Chinese medicine for conditions such as fatigue, neurosis (neurasthenia), and spontaneous sweating, has recently been the subject of rigorous scientific investigations regarding its potential to modulate the immune system. A particularly significant study, published in the journal Molecules in 2011, entitled “The immuno-regulatory effects of Schisandrachinensis and its constituents on human monocytic leukemia cells” (PMID/PMC accessible), examined in vitro the impact of two major lignans—schizandrin (Sch) and gomisin A (Gom A)—on human monocyte-leukemia cells (THP-1 cell line). PubMed +1Study Context and Objectives
This study is based on the premise that the activation or modulation of immune cells (here, monocytes/macrophages) via cytokine release is a central mechanism in the host immune response. The authors emphasize that immunosuppression is implicated in a large number of pathologies, and that nutritional or phytochemical agents capable of stimulating or regulating this response are of increasing interest.
PMC+1 Until now, the traditional use of S. chinensis as a “tonic” lacked precise molecular explanations for its immune effects. The objective was therefore to evaluate whether isolated constituents of the plant could modulate cytokine release by THP-1 cells and, thereby, induce an adaptive or innate (humoral and cellular) immune response.
Methodology The authors extracted a 95% ethanol extract from S. chinensis and then isolated two lignans, schizandrin and gomisinA, which were identified by HPLC chromatography.PMC+2
MDPI +2THP-1 cells (human monocytic leukemia cell line) were treated with these compounds at various concentrations (up to 100 µM). A first-step toxicity test (MTT) confirmed that at the concentrations used, cell viability remained high (>90% at 100 µM): schizandrin ≈ 102.6% viability, gomisin A ≈ 93.2% (100 µM) as measured.
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+1 Next, cytokine release was measured by flow cytometry multiplex for certain mediators: IL-8, GM-CSF (granulocyte-macrophage-colony stimulating factor), and MIP-1β (macrophage inflammatory protein-1β).
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Concurrently, the expression of the corresponding mRNAs was quantified via RT-PCR or qRT-PCR (for IL-8, MIP-1β, GM-CSF) in the cells after treatment. MDPI +1
Key Results The study showed that both schizandrin and gomisin A induced a significant increase in the release of IL-8 and MIP-1β, and to a lesser extent GM-CSF, by THP-1 cells. For example, according to flow cytometry data: at 100 µM, there was an increase in IL-8 of 136.21 ± 24.10 pg/mL for schizandrin and 67.15 ± 1.48 pg/mL for gomisin A (compared to the mean control) — data taken from the published table.
PMC The release of MIP-1β was also increased (24.49 ± 5.97 pg/mL for Sch at 100 µM, 21.30 ± 1.79 pg/mL for Gomisin A).
At the mRNA level: Schizandrin 100 µM had an IL-8/GAPDH ratio of approximately 1.73 (vs. control) and a MIP-1β/GAPDH ratio of approximately 1.49 according to RT-PCR. By qRT-PCR, schizandrin induced a factor of approximately 1.90 in MIP-1β mRNA. Gomisin A also showed dose-dependent induction: 2.71-, 2.56-, 1.99-fold (100, 80, 60 µM) for MIP-1β according to qRT-PCR.
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The authors conclude that S. chinensis, through its lignans, can promote both humoral and cellular immunity—notably via the activation of key cytokines and the potential differentiation/hematopoiesis of cells in the monocytic lineage.
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However, the lack of evaluation of all cytokines (e.g., IL-6, TNF-α, IFN-γ) or of studies in human conditions limits generalization. It should also be noted that the study focuses on a leukemia cell line (THP-1), which may not fully replicate the behavior of healthy circulating monocytes. Finally, an increase in cytokines is not always beneficial: an excess or inappropriate activation could lead to chronic inflammation or immune dysfunction. Therefore, these effects should be considered within the framework of regulated modulation rather than raw stimulation.
Limitations and points for further investigation
Several limitations should be noted:
The in vitro model (THP-1) does not replace an in vivo human or animal study with a complete immune system.
The study dates from 2011, which implies that further research is needed to confirm efficacy and safety.
