Evidence Details for Grk2
PMID Title Journal Year Abstract
26064176 Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture. Evid Based Complement Alternat Med. 2015;2015:848603. doi: 10.1155/2015/848603. Epub 2015 Apr 29. 2015 Acupuncture or electroacupuncture (EA) has been demonstrated to have a powerful antihypernociceptive effect on inflammatory pain. The attenuation of G protein-coupled receptor kinase 2 (GRK2) in spinal cord and peripheral nociceptor has been widely acknowledged to promote the transition from acute to chronic pain and to facilitate the nociceptive progress. This study was designed to investigate the possible role of spinal GRK2 in EA antiallodynic in a rat model with complete Freund's adjuvant (CFA) induced inflammatory pain. EA was applied to ST36 (""Zusanli"") and BL60 (""Kunlun"") one day after CFA injection. Single EA treatment at day 1 after CFA injection remarkably alleviated CFA induced mechanical allodynia two hours after EA. Repeated EA displayed significant antiallodynic effect from 2nd EA treatment and a persistent effect was observed during the rest of treatments. However, downregulation of spinal GRK2 by intrathecal exposure of GRK2 antisense 30 mins after EA treatment completely eliminated both the transient and persistent antiallodynic effect by EA treatment. These pieces of data demonstrated that the spinal GRK2 played an important role in EA antiallodynia on inflammatory pain."

Evidence Sentence: The attenuation of G protein-coupled receptor kinase 2 (GRK2) in spinal cord and peripheral nociceptor has been widely acknowledged to promote the transition from acute to chronic pain and to facilitate the nociceptive progress.
Evidence Sentence: This study was designed to investigate the possible role of spinal GRK2 in EA antiallodynic in a rat model with complete Freund's adjuvant (CFA) induced inflammatory pain.
Evidence Sentence: However, downregulation of spinal GRK2 by intrathecal exposure of GRK2 antisense 30 mins after EA treatment completely eliminated both the transient and persistent antiallodynic effect by EA treatment.
Evidence Sentence: These pieces of data demonstrated that the spinal GRK2 played an important role in EA antiallodynia on inflammatory pain.
Evidence Sentence: The Role of Spinal GRK2 in EA Anti-Allodynic Effect
Evidence Sentence: treatment with GRK2 AS-ODN for three consecutive days showed a significant decrease in GRK2 protein levels in the spinal cord as compared to MM-ODN group (Figures 3(a) and 3(b)).
Evidence Sentence: injection of GRK2 AS-ODN as compared to MM-ODN treated rats or CFA rats without any treatment (Figures 3(c) and 3(d)).
Evidence Sentence: Single GRK2 AS-ODN i.t.
Evidence Sentence: And repeated GRK2 AS-ODN exposure suppressed the long-term antiallodynic effect of EA during all the experiments (Figure 3(d)).
Evidence Sentence: But GRK2 MM-ODN delivery displayed no effect on the mechanical threshold after EA treatment as compared to CFA rats.
Evidence Sentence: Furthermore, neither GRK2 AS-ODN nor MM-ODN changed the PWT on normal rats (Figures 3(e) and 3(f)).
Evidence Sentence: These pieces of data suggested that the attenuation of spinal GRK2 completely eliminated the antiallodynic effect of EA treatment.
Evidence Sentence: But, the expression level of GRK2 did not affect nociception in physiological conditions.