Anti-Inflammatory Effects of Acupuncture in the Treatment of Chronic Obstructive Pulmonary Disease

This narrative review offers a comprehensive analysis of the anti-inflammatory mechanisms of acupuncture in the treatment of chronic obstructive pulmonary disease (COPD), based on 27 studies with animal models. COPD is characterized by persistent chronic inflammation that affects both the lungs and causes systemic manifestations, representing an important global health problem. The methodology of the reviewed studies primarily used rats as an animal model, with COPD induced through cigarette smoke exposure combined with lipopolysaccharide (LPS), a method that adequately reproduces the inflammatory characteristics of human disease. Electroacupuncture emerged as the most used modality in the studies, with typical parameters of 4/20 Hz or 10/50 Hz, intensity of 1–3 mA, and sessions of 20–30 minutes.

The most frequently selected acupoints were Feishu (BL-13) and Zusanli (ST-36), appearing in 19 and 18 studies, respectively, establishing themselves as fundamental core points in experimental COPD treatment. The results demonstrate that acupuncture exerts robust anti-inflammatory effects through multiple mechanisms. First, it significantly reduces the infiltration of inflammatory cells such as neutrophils, macrophages, monocytes, and lymphocytes in lung tissues. Second, it regulates the polarization of alveolar macrophages, inhibiting pro-inflammatory M1 polarization and promoting the anti-inflammatory M2 phenotype.

Third, it modulates the Th1/Th2 balance, contributing to a more balanced immune response. The identified molecular mechanisms involve four main signaling pathways. The NF-κB pathway, including the MyD88/NF-κB, TLR-4/NF-κB, and SIRT1/NF-κB sub-pathways, represents the central mechanism for regulating inflammatory gene transcription. The MAPK pathway (mitogen-activated protein kinases), including ERK1/2, JNK, and p38, mediates cellular responses to inflammation.

The cholinergic anti-inflammatory pathway (CAP) connects the nervous system to inflammation control through vagal modulation. Finally, the dopamine D2 receptor pathway represents an innovative neuroimmunological mechanism in which acupuncture increases dopamine levels, which in turn inhibit NLRP3 inflammasome activation. The study also revealed that acupuncture consistently regulates inflammatory cytokines, decreasing pro-inflammatory markers such as TNF-α, IL-1β, IL-6, IL-8, and IFN-γ, while increasing the anti-inflammatory cytokine IL-10. Interestingly, different types of acupuncture (electroacupuncture, manual, acupoint application) showed similar efficacy in modulating these cytokines, suggesting that the anti-inflammatory effect is an inherent characteristic of acupoint stimulation, regardless of the specific modality.

The review also identified epigenetic mechanisms, in which acupuncture regulates HDAC2 (histone deacetylase 2) expression, suppressing the transcription of pro-inflammatory genes. In addition, neurotransmitters such as orexin, CGRP, and serotonin are modulated by acupuncture, creating an integrated neuroimmunological effect. The clinical implications are significant, as they provide a robust scientific basis for the use of acupuncture as adjuvant therapy in COPD. Acupuncture's ability to modulate multiple inflammatory pathways simultaneously offers advantages over therapies that target only one molecular target.

Limitations include the need for validation in controlled clinical studies, better understanding of the interactions between different signaling pathways, and development of standardized protocols for different COPD phenotypes.