scholarly journals An Hypothesis for CXCL1/CXCR2 Signaling Regulating Neutrophil-Derived Opioid Peptides Involved in Acupuncture for Inflammatory Pain

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Sha-sha Ding ◽  
Yuan Xu ◽  
Ying-ying Zhang ◽  
Jing-zi Chen ◽  
Shou-hai Hong

Increasing evidences demonstrate that acupuncture is effective in treating inflammatory pain. Recent studies have found that peripheral endogenous opioid peptides in the area of inflammation are involved in acupuncture-treating inflammatory pain. However, the source of endogenous opioid peptides in local area of inflammation and the mechanism of acupuncture regulating these opioid peptides remain unclear. Studies have demonstrated that neutrophils infiltrated in the inflamed tissue contain and release opioid peptides. Chemokine (C-X-C motif) ligand 1 (CXCL1) is one of the key neutrophil chemokines and can promote the blood neutrophil recruitment to the area of inflammation. In our previous experiments, we found that acupuncture could alleviate inflammatory pain and significantly increase the concentration of chemokine CXCL1 in the blood of rats with inflammatory pain. So we suppose that increased concentration of CXCL1 by acupuncture could activate the blood opioid-containing neutrophils via its main receptor chemokine receptor type 2 (CXCR2) and promote them recruit to the inflamed tissue to release opioid peptides, participating in the analgesic effect of acupuncture.

The Lancet ◽  
1993 ◽  
Vol 342 (8867) ◽  
pp. 321-324 ◽  
Author(s):  
C. Stein ◽  
A.H.S. Hassan ◽  
K. Lehrberger ◽  
C. Stein ◽  
J. Giefing ◽  
...  

1994 ◽  
Vol 38 (4) ◽  
pp. 221
Author(s):  
C. STEIN ◽  
A. H. S. HASSAN ◽  
K. LEHRBERGER ◽  
J. GIEFING ◽  
A. YASSOURIDIS

1987 ◽  
Vol 72 (s16) ◽  
pp. 90P-91P
Author(s):  
J.R. Thornton ◽  
M.S. Losowsky

1999 ◽  
Vol 277 (6) ◽  
pp. H2442-H2450 ◽  
Author(s):  
Yasushi Takasaki ◽  
Roger A. Wolff ◽  
Grace L. Chien ◽  
Donna M. van Winkle

In rats and rabbits, endogenous opioid peptides participate in ischemic preconditioning. However, it is not known which endogenous opioid(s) can trigger cardioprotection. We examined preconditioning-induced and opioid-induced limitation of cell death in isolated, calcium-tolerant, adult rabbit cardiomyocytes. Cells were subjected to simulated ischemia by pelleting and normothermic hypoxic incubation. Preconditioning was elicited with 15 min of simulated ischemia followed by 15 min of resuspension and reoxygenation. All cells underwent 180 min of simulated ischemia. Cell death was assessed by trypan blue permeability. Morphine protected cells, as did preconditioning; naloxone blocked the preconditioning-induced protection. Exogenous Met5-enkephalin (ME) induced protection, but exogenous β-endorphin did not. ME-induced protection was blocked by the δ-selective antagonist naltrindole. Additionally, two other proenkephalin products, Leu5-enkephalin and Met5-enkephalin-Arg-Phe, provided protection equipotent to ME. These data suggest that one or more proenkephalin products interact with δ-opioid receptors to endogenously trigger opioid-mediated protection.


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