Lung cancer is the leading cause of cancer‐related death worldwide, and non–small cell lung cancer (NSCLC) accounts for 85% of lung cancer diagnoses. As an ancient therapy, moxibustion has been used to treat cancer‐related symptoms in clinical practice. However, its antitumour effect on NSCLC remains largely unexplored. In the present study, a Lewis lung cancer (LLC) xenograft tumour model was established, and grain‐sized moxibustion (gMoxi) was performed at the acupoint of Zusanli (ST36). Flow cytometry and RNA sequencing (RNA‐Seq) were used to access the immune cell phenotype, cytotoxicity and gene expression. PK136, propranolol and epinephrine were used for natural killer (NK) cell depletion, β‐adrenoceptor blockade and activation, respectively. Results showed that gMoxi significantly inhibited LLC tumour growth. Moreover, gMoxi significantly increased the proportion, infiltration and activation of NK cells, whereas it did not affect CD4⁺and CD8⁺T cells. NK cell depletion reversed gMoxi‐mediated tumour regression. LLC tumour RNA‐Seq indicated that these effects might be related to the inhibition of adrenergic signalling. Surely, β‐blocker propranolol clearly inhibited LLC tumour growth and promoted NK cells, and gMoxi no longer increased tumour regression and promoted NK cells after propranolol treatment. Epinephrine could inhibit NK cell activity, and gMoxi significantly inhibited tumour growth and promoted NK cells after epinephrine treatment. These results demonstrated that gMoxi could promote NK cell antitumour immunity by inhibiting adrenergic signalling, suggesting that gMoxi could be used as a promising therapeutic regimen for the treatment of NSCLC, and it had a great potential in NK cell–based cancer immunotherapy.

Background: Moxibustion, a traditional Chinese medicine (TCM) therapy, employs thermal stimulation from the combustion of Artemisia argyi H.Lév. & Vaniot at acupoints to treat "deficiency-cold syndromes" (xuhan zheng), historically linked to immune dysfunction and chronic inflammation. Modern pharmacological studies showed that grain-sized moxibustion (gM) enhances innate immune surveillance such as natural killer (NK) cell recruitment. However, its synergy with vaccine-induced adaptive immunity remains unexplored. Guided by the TCM principle of fu zheng qu xie (“fortify the host to dispel pathogens”), this study investigated whether gM augments cancer vaccine efficacy and validate the mechanistic basis of thermal acupoint stimulation in amplifying adaptive antitumor immunity. Methods: In tumor-bearing mice model, gM was applied to the ST36 (Zusanli) acupoint. Adjuvant effects on the cancer vaccine were evaluated through flow cytometry, β-adrenergic receptor blockade, and cell depletion. Results: gM synergized with the cancer vaccine, significantly suppressing tumor growth. Mechanistically, gM inhibited β-adrenergic signaling, driving DC maturation and subsequent coordination of CD4⁺ T cell, CD8⁺ T cell and NK cell responses. CD4⁺ T cells as primary effectors, with NK cells playing a secondary role. Propranolol mirrored gM’s effects, further enhancing DC activation and tumor suppression when combined with vaccination. Conclusion: Both gM and β-blockers enhance cancer vaccine efficacy through β-adrenergic suppression and maturation of DC. These findings mechanistically bridge TCM’s fu zheng qu xie strategy with modern immunotherapy, positioning β-adrenergic modulation as a convergent target for traditional and pharmacological interventions.

The persistence of neuronal degeneration and damage is a major obstacle in ageing medicine. Nucleotide-binding oligomerization domain (NOD)-like receptors detect environmental stressors and trigger the maturation and secretion of pro-inflammatory cytokines that can cause neuronal damage and accelerate cell death. NLR (NOD-like receptors) inflammasomes are protein complexes that contain NOD-like receptors. Studying the role of NLR inflammasomes in ageing-related neurological disorders can provide valuable insights into the mechanisms of neurodegeneration. This includes investigating their activation of inflammasomes, transcription, and capacity to promote or inhibit inflammatory signaling, as well as exploring strategies to regulate NLR inflammasomes levels. This review summarizes the use of NLR inflammasomes in guiding neuronal degeneration and injury during the ageing process, covering several neurological disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, stroke, and peripheral neuropathies. To improve the quality of life and slow the progression of neurological damage, NLR-based treatment strategies, including inhibitor-related therapies and physical therapy, are presented. Additionally, important connections between age-related neurological disorders and NLR inflammasomes are highlighted to guide future research and facilitate the development of new treatment options.