ArticleJournal of medical biochemistry2025
Acceptance and Commitment Therapy modulates immuneinflammatory responses and neurotrophic factors homeostasis in elderly stroke patients: A randomized controlled trial.
Article in Journal of medical biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: 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. Methods: 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. Results: 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< 0.05). Proinflammatory cytokine levels (IL-1 b, IL-6, and TNF-a) were significantly suppressed, whereas anti-inflammatory IL-10 expression increased (P < 0 .0 5 ). Notably, ACT demonstrated superior efficacy in restoring immune balance and attenuating inflammation compared to conventional intervention (P< 0.05). Furthermore, neurotrophic factors levels were elevated, and oxidative stress markers were ameliorated in CS after treatment (P< 0.05), suggesting that ACT enhances neurotrophic activity and mitigates oxidative injury. Conclusions: ACT likely confers neuroprotection through multi-target mechanisms, including modulation of T-cell subset homeostasis, upregulation of neurotrophic factors, and suppression of oxidative stress.
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