ArticleJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2026
Regulatory effects and mechanisms of the acupuncture-induced complement component 1q on the high mobility group box 1 -receptor for advanced glycation end products-nuclear factor kappa-B pathway at Zusanli (ST36).
Article in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 2026. 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
objectiveTo investigate what are the crucial regulators and mechanisms involved in regulating the inflammatory responses at Zusanli (ST36).
methodsInitially, we utilized enzyme-linked immunosorbent assay (ELISA) to detect the variations of high mobility group box 1 (HMGB1), interleukin-10 (IL-10), and complement component 1q (C1q) concentrations at Zusanli (ST36) on day 1 (D1), day 3 (D3), day 5 (D5) and day 7 (D7) after acupuncture to clearly depict the time-dependent changes of these inflammatory substances. Subsequently, we utilized C1qa-knockout (C1qa-KO) mice to investigate the role of acupuncture-induced C1q in inflammatory responses at Zusanli (ST36). We utilized hematoxylin and eosin staining to observe the inflammatory morphological alterations, examined the activation of the NF-κB pathway by immunofluorescence and assessed HMGB1 and IL-10 changes using ELISA. Lastly, to uncover the specific mechanism by which C1q regulates the acupuncture-induced inflammatory responses at Zusanli (ST36), we employed Western blot (WB) to measure the expression levels of receptor of advanced glycation end products (RAGE), leukocyte associated immunoglobulin like receptor 1 (LAIR-1), and src homology region 2 domain-containing protein tyrosine phosphatase 1 (SHP-1) proteins and used immunofluorescence to detect the polarization of classically activated macrophages (M1) and alternatively activated macrophages (M2).
resultsCompared with the wild-type group, the levels of HMGB1 and C1q of acupuncture (ACU) group at Zusanli (ST36) were increased on D3 after acupuncture, while the level of IL-10 decreased. With continued higher level of HMGB1, both C1q and IL-10 level were increased on D7. After knocking out C1q, compared with the ACU group, the C1qa-KO+acupuncture (C1q
conclusionZusanli (ST36) acupuncture initiates a time-regulated inflammatory cascade might through the following mechanism: HMGB1 release (D1) triggers C1q upregulation (D3), culminating on D7 with C1q binding to LAIR-1, which recruits SHP-1 to inhibit HMGB1-RAGE-NF-κB signaling
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