Abstract
So far, a number of acupuncture studies have shown anti-inflammatory effects of acupuncture treatment, mostly known at specific point ST36. However, there is no literature that oversaw the inflammation-regulatory effects of acupuncture in each tissue. Therefore, we investigated how acupuncture at specific acupoint ST36 regulates inflammation and its underlying mechanisms. We searched literatures on PubMed until July 2021 using the keywords “animal, acupuncture, ST36, inflammation, immune,” and 292 literatures were searched. We ultimately selected 69 studies to determine the anti-inflammatory actions of acupuncture at ST36 and classified the changes of inflammatory mediators according to target regions. Forty-three studies were included in body fluids, 27 studies in the digestive system, 17 studies in the nervous system, and 30 studies in other tissues or organs. In this review, we found that acupuncture at ST36 has clinical benefits in relieving inflammation through several mechanisms such as vagus nerve activation, toll-like receptor 4 (TLR4)/NF-κB signaling, macrophage polarization, mitogen-activated protein kinase (MAPK) signaling pathway, and cholinergic anti-inflammatory pathway. We expect that these data will inform further studies related to ST36 acupuncture on inflammation.
Highlights
Inflammation is a physiological protective process that prevents foreign injuries or infections
Since there is no literature review that organized the effects of acupuncture at ST36 on the whole inflammatory models, we totally investigated the inflammation-related biomarkers in target regions and suggested that acupuncture at ST36 could be a clinical treatment of inflammatory disorders
In order to oversee how acupuncture regulates systemic inflammation, we investigated the change of inflammatory mediators in body fluids
Summary
Inflammation is a physiological protective process that prevents foreign injuries or infections. Inflammation includes an inflammatory response and the step of restoring tissues. The biological progression of inflammation is composed of diverse inflammatory cytokines and chemokines. Tumor necrosis factor-a (TNF-a) is produced by inflammatory cells and induces encoding genes of antiapoptotic molecules. IL-6 is one of the inflammatory cytokines, and STAT3 plays a critical role in its signal transduction (1). Immune cells are deeply involved in the inflammation triggered by external or endogenous stimuli. Macrophages play a critical role in the maintenance of tissue homeostasis and are composed of two subsets: M1 macrophages, which produce proinflammatory cytokines, and M2 macrophages, which promote tissue repairs and secrete inflammation-suppressive mediators (2). Since prolonged chronic inflammation can lead to irreparable damage to tissues and aggravate the disease status, operation of the rapid immune system and normal regulation of inflammatory mediators is important (4)
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