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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. |
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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. |
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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. |
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These pieces of data demonstrated that the spinal GRK2 played an important role in EA antiallodynia on inflammatory pain. |
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The Role of Spinal GRK2 in EA Anti-Allodynic Effect |
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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)). |
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injection of GRK2 AS-ODN as compared to MM-ODN treated rats or CFA rats without any treatment (Figures 3(c) and 3(d)). |
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Single GRK2 AS-ODN i.t. |
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And repeated GRK2 AS-ODN exposure suppressed the long-term antiallodynic effect of EA during all the experiments (Figure 3(d)). |
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But GRK2 MM-ODN delivery displayed no effect on the mechanical threshold after EA treatment as compared to CFA rats. |
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Furthermore, neither GRK2 AS-ODN nor MM-ODN changed the PWT on normal rats (Figures 3(e) and 3(f)). |
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These pieces of data suggested that the attenuation of spinal GRK2 completely eliminated the antiallodynic effect of EA treatment. |
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But, the expression level of GRK2 did not affect nociception in physiological conditions. |