# Acceptance and Commitment Therapy modulates immuneinflammatory responses and neurotrophic factors homeostasis in elderly stroke patients: A randomized controlled trial

**Authors:** Jing Wang, Haiyan Gu, Xiaorong Hu, Yanjie Zhou, Lingling Wu

PMC · DOI: 10.5937/jomb0-58244 · Journal of Medical Biochemistry · 2025-11-05

## TL;DR

This study shows that Acceptance and Commitment Therapy (ACT) helps elderly stroke patients by improving immune balance, reducing inflammation, and boosting brain repair factors.

## Contribution

The study demonstrates that ACT has multi-target effects on immune, inflammatory, and neurotrophic pathways in elderly stroke patients.

## Key findings

- ACT reduced proinflammatory cytokines and increased anti-inflammatory IL-10 in stroke patients.
- ACT improved T-cell subset balance and elevated neurotrophic factors like BDNF and IGF-1.
- ACT mitigated oxidative stress by reducing lipid peroxidation markers and enhancing antioxidant enzymes.

## Abstract

This study examined the regulatory effects of Acceptance and Commitment Therapy (ACT) on T lymphocyte subsets, serum inflammatory cytokines, neurotrophic factors, antioxidant enzymes, and lipid peroxidation products in elderly cerebral stroke (CS) patients, providing insights into the multi-dimensional pathophysiological interactions and potential intervention strategies for chronic stroke recovery.

In this randomized controlled trial, 120 elderly stroke patients were allocated to either an ACT group (ACT intervention; n = 60) or a routine group (conventional treatment; n = 60). Comprehensive assessments were performed to quantify: (1) peripheral T lymphocyte distribution (CD3+, CD4+, CD8+ subsets, and CD4+/CD8+ ratio), (2) serum inflammatory cytokines (IL-1p, IL-6, IL-10, and TNF-a), (3) neurotrophic factors (5-HT, NE, BDNF, and IGF-1), and (4) antioxidant enzymes (SOD, CAT) and lipid peroxidation products (MDA, NO) using flow cytometry, HPLC-ECD, and ELISA. Statistical analyses were conducted with SPSS 22.0.

Following treatment, CS patients exhibited reduced CD3+ and CD4+ T-cell levels along with a decreased CD4+/CD8+ ratio, while CD8+ T-cell proportions were elevated (P&lt; 0.05). Proinflammatory cytokine levels (IL-1 b, IL-6, and TNF-a) were significantly suppressed, whereas anti-inflammatory IL-10 expression increased (P &lt; 0 .0 5 ). Notably, ACT demonstrated superior efficacy in restoring immune balance and attenuating inflammation compared to conventional intervention (P&lt; 0.05). Furthermore, neurotrophic factors levels were elevated, and oxidative stress markers were ameliorated in CS after treatment (P&lt; 0.05), suggesting that ACT enhances neurotrophic activity and mitigates oxidative injury.

ACT likely confers neuroprotection through multi-target mechanisms, including modulation of T-cell subset homeostasis, upregulation of neurotrophic factors, and suppression of oxidative stress.

## Linked entities

- **Proteins:** BDNF (brain derived neurotrophic factor), IGF1 (insulin like growth factor 1), SOD1 (superoxide dismutase 1), CAT (catalase), so (sine oculis), Nos1 (nitric oxide synthase 1, neuronal)

## Full-text entities

- **Genes:** BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, NTRK2 (neurotrophic receptor tyrosine kinase 2) [NCBI Gene 4915] {aka DEE58, EIEE58, GP145-TrkB, OBHD, TRKB, trk-B}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, HMOX1 (heme oxygenase 1) [NCBI Gene 3162] {aka HMOX1D, HO-1, HSP32, bK286B10}, FOXP3 (forkhead box P3) [NCBI Gene 50943] {aka AIID, DIETER, IPEX, JM2, PIDX, XPID}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, IL2RA (interleukin 2 receptor subunit alpha) [NCBI Gene 3559] {aka CD25, IDDM10, IL2R, IMD41, TCGFR, p55}, DLG4 (discs large MAGUK scaffold protein 4) [NCBI Gene 1742] {aka MRD62, PSD95, SAP-90, SAP90}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, NOX4 (NADPH oxidase 4) [NCBI Gene 50507] {aka KOX, KOX-1, RENOX}, IGF1R (insulin like growth factor 1 receptor) [NCBI Gene 3480] {aka CD221, IGFIR, IGFR, JTK13}, MAPK8 (mitogen-activated protein kinase 8) [NCBI Gene 5599] {aka JNK, JNK-46, JNK1, JNK1A2, JNK21B1/2, PRKM8}, MAPK1 (mitogen-activated protein kinase 1) [NCBI Gene 5594] {aka ERK, ERK-2, ERK2, ERT1, MAPK2, NS13}, FASLG (Fas ligand) [NCBI Gene 356] {aka ALPS1B, APT1LG1, APTL, CD178, CD95-L, CD95L}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, FAS (Fas cell surface death receptor) [NCBI Gene 355] {aka ALPS1A, APO-1, APT1, CD95, FAS1, FASTM}, CAT (catalase) [NCBI Gene 847], APC (APC regulator of Wnt signaling pathway) [NCBI Gene 324] {aka BTPS2, DESMD, DP2, DP2.5, DP3, GS}
- **Diseases:** personality disorders (MESH:D010554), CS (MESH:D020521), neuronal damage (MESH:D009410), cerebral edema (MESH:D001929), Depression (MESH:D003866), chronic pain (MESH:D059350), cognitive impairment (MESH:D003072), neuronal apoptosis (MESH:D065703), motor dysfunction (MESH:D000068079), immune dysregulation (OMIM:614878), neuroendocrine disturbances (MESH:D018358), inflammation (MESH:D007249), neurodegeneration (MESH:D019636), Symptom (MESH:D012816), cytotoxicity (MESH:D064420), neuroinflammation (MESH:D000090862), Anxiety (MESH:D001007), neural deterioration (MESH:D015441), neurotoxicity (MESH:D020258), ACT (MESH:D016609), Alzheimer's disease (MESH:D000544), cardiopulmonary failure (MESH:D051437), mental illness (MESH:D001523), malignant tumors (MESH:D009369), ischemic (MESH:D002545)
- **Chemicals:** lipid (MESH:D008055), ATP (MESH:D000255), aspirin (MESH:D001241), NO (MESH:D009569), 5-HT (MESH:D012701), ROS (MESH:D017382), PBS (MESH:D007854), GABA (MESH:D005680), NE (MESH:D009356), phosphate (MESH:D010710), ACT (-), hydrogen peroxide (MESH:D006861), NO (MESH:D009614), methanol (MESH:D000432), MDA (MESH:D008315), DA (MESH:C025953), MDA (MESH:D015104), EDTA (MESH:D004492)
- **Species:** Homo sapiens (human, species) [taxon 9606]

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## References

29 references — full list in the complete paper: https://tomesphere.com/paper/PMC12967185/full.md

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Source: https://tomesphere.com/paper/PMC12967185