Evidence Details for Iba1
PMID Title Journal Year Abstract
35656078 Acupuncture points injection mitigates chronic pain through transient receptor potential V1 in mice. Iran J Basic Med Sci. 2022 Apr;25(4):451-459. doi: 10.22038/IJBMS.2022.60121.13327. 2022 Apr OBJECTIVES: Tissue injury in peripheral sites can result in long-term potentiation in nociceptive neurons and surrounding glial cells, potentially resulting in the development of chronic inflammatory pain (CIP). Acupoint injection (AI) is similar to Western phototherapy, which injects solutions at specific sites to mitigate chronic pain. AI has shown greater benefits compared with acupuncture. In this study, we examined the therapeutic effect and explored the underlying mechanisms of AI in mice CIP model. MATERIALS AND METHODS: We injected thrice complete Freund's adjuvant (CFA) into the mouse's hind paw to induce CIP. RESULTS: We found that, after two weeks, CFA injection significantly induced mechanical and thermal hyperalgesia which were attenuated by AI treatment. Transient receptor potential V1 (TRPV1) channels and associated molecules were all increased in CIP in mice dorsal root ganglion (DRG), spinal cord (SC), thalamus, and somatosensory cortex (SSC). The aforementioned molecules were mitigated in AI and Trpv1 knockout mice. Furthermore, Iba1-positive cells (microglial marker) were also potentiated and shared a similar tendency with TRPV1. CONCLUSION: These findings suggest that AI can alleviate chronic pain by reducing TRPV1 overexpression in both neuronal and microglial cells. Our results suggest new potential therapeutic targets for AI in chronic pain."

Evidence Sentence: Furthermore, Iba1-positive cells (microglial marker) were also potentiated and shared a similar tendency with TRPV1.
Evidence Sentence: Finally, the activated microglial markers Iba1 (Figure 2N), S100B (Figure 2O), and RAGE (Figure 2P) were also elevated by CIP, and these responses were reversed by AI and lower in CIP model Trpv1-/- mice than CIP model WT mice.
Evidence Sentence: In accordance with findings in DRG and SC, there were significant increases in the expression levels of TRPV1 (Figures 4A, 5A), pPKA (Figures 4B, 5B), pPI3K (Figures 4C, 5C), pPKC (Figures 4D, 5D), pERK (Figures 4E, 5E), pJNK (Figures 4F, 5F), pp38 (Figures 4G, 5G), pAkt (Figures 4H, 5H), pmTOR (Figures 4I, 5I), pCREB (Figures 4J, 5J), pNFkappaB (Figures 4K, 5K), Nav1.7 (Figures 4L, 5L), Nav1.8 (Figures 4M, 5M), Iba1 (Figure 4N, 5N), S100B (Figure 4O, 5O), and RAGE (Figures 4P, 5P) following CIP induction.
Evidence Sentence: Immunofluorescence staining also confirmed elevated expression of the glial cell marker Iba1 in the DRG following CIP induction, which was attenuated by AI treatment and Trpv1 gene deletion (Figure 6B).
Evidence Sentence: Further, TRPV1 and Iba1 were colocalized in CIP model mice, indicating that the elevation in tissue TRPV1 was mediated by increased expression in DRG glial cells.
Evidence Sentence: Similar changes in TRPV1 and Iba1 expression were also observed in the somatosensory cortex (Figure 7).
Evidence Sentence: Co-expression of TRPV1 and Iba1 in cells of the thalamusand somatosensory cortex
Evidence Sentence: Finally, we examined these changes in cellular TRPV1 and Iba1 in the thalamus (Figure 8) and somatosensory cortex (Figure 9).
Evidence Sentence: In accord with western blotting and other immunofluorescence results, TRPV1 immunoreactivity (Figure 8A) and Iba1 immunoreactivity (Figure 8B) were elevated concomitantly by CIP induction.
Evidence Sentence: Further, these elevated expression levels were reversed by AI (Figures 8A and 8B, respectively), while Iba1 expression was lower in CIP model Trpv1-/- mice than WT mice (Figure 8C).
Evidence Sentence: In the somatosensory cortex as well, TRPV1, Iba1, and TRPV1/Iba1 co-staining signals were all increased in CIP model mice and reversed by AI (Figure 9).
Evidence Sentence: Further, the changes in Iba1 were suppressed in Trpv1-/- mice.