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Effect of Repeated Electroacupuncture Intervention on Hippocampal ERK and p38MAPK Signaling in Neuropathic Pain Rats.

Wang JY, Chen SP, Gao YH, Qiao LN, Zhang JL, Liu JL - Evid Based Complement Alternat Med (2015)

Bottom Line: After CCI, the thermal pain thresholds of the affected hind were significantly decreased compared with the control group (P < 0.05).Following one and two weeks' EAS of ST 36-GB34, the pain thresholds were significantly upregulated (P < 0.05), and the effect of EA2W was remarkably superior to that of EA2D and EA1W (P < 0.05).The above mentioned results indicated that EA2W induced cumulative analgesic effect may be closely associated with its function in removing neuropathic pain induced suppression of intracellular ERK and p38MAPK signaling in the hippocampus.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Beijing 100700, China.

ABSTRACT
Results of our past studies showed that hippocampal muscarinic acetylcholine receptor (mAChR)-1 mRNA and differentially expressed proteins participating in MAPK signaling were involved in electroacupuncture (EA) induced cumulative analgesia in neuropathic pain rats, but the underlying intracellular mechanism remains unknown. The present study was designed to observe the effect of EA stimulation (EAS) on hippocampal extracellular signal-regulated kinases (ERK) and p38 MAPK signaling in rats with chronic constrictive injury (CCI) of the sciatic nerve, so as to reveal its related intracellular targets in pain relief. After CCI, the thermal pain thresholds of the affected hind were significantly decreased compared with the control group (P < 0.05). Following one and two weeks' EAS of ST 36-GB34, the pain thresholds were significantly upregulated (P < 0.05), and the effect of EA2W was remarkably superior to that of EA2D and EA1W (P < 0.05). Correspondingly, CCI-induced decreased expression levels of Ras, c-Raf, ERK1 and p-ERK1/2 proteins, and p38 MAPK mRNA and p-p38MAPK protein in the hippocampus tissues were reversed by EA2W (P < 0.05). The above mentioned results indicated that EA2W induced cumulative analgesic effect may be closely associated with its function in removing neuropathic pain induced suppression of intracellular ERK and p38MAPK signaling in the hippocampus.

No MeSH data available.


Related in: MedlinePlus

Effect of EA on expression levels of hippocampal MEK, p-MEK proteins in different groups. Data are presented as mean ± SD (∗P < 0.05, compared with the sham control group; n = 5 in each group). (a) Upper panel shows representative immunoblots of MEK protein in the 5 groups: (1) sham control group, (2) CCI group, (3) CCI + EA2D group, (4) CCI + EA1W group, and (5) CCI + EA2W group; lower histograms show the relative expression levels of MEK protein in the 5 groups. (b) The lower histograms show the relative expression levels of p-MEK1 and p-MEK2 proteins in the five groups; upper panel shows the representative immunoblots of MEK1/2 proteins and GAPDH in different groups.
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fig3: Effect of EA on expression levels of hippocampal MEK, p-MEK proteins in different groups. Data are presented as mean ± SD (∗P < 0.05, compared with the sham control group; n = 5 in each group). (a) Upper panel shows representative immunoblots of MEK protein in the 5 groups: (1) sham control group, (2) CCI group, (3) CCI + EA2D group, (4) CCI + EA1W group, and (5) CCI + EA2W group; lower histograms show the relative expression levels of MEK protein in the 5 groups. (b) The lower histograms show the relative expression levels of p-MEK1 and p-MEK2 proteins in the five groups; upper panel shows the representative immunoblots of MEK1/2 proteins and GAPDH in different groups.

Mentions: MEK1/2 (MKK1/2) are the upstream kinases of ERK signaling. Compared with the control group, the expression levels of hippocampal MEK and p-MEK1 proteins had no significant changes in the CCI, CCI + EA2D, CCI + EA1W, and CCI + EA2W groups (P > 0.05, Figure 3(a)), while that of p-MEK2 protein was significantly downregulated after CCI (P < 0.05, Figure 3(b)). Following EAS of ST36-GB34, p-MEK2 expression had a slight upregulation in the three EAS groups (P > 0.05) without significant differences among the three groups (P > 0.05).


Effect of Repeated Electroacupuncture Intervention on Hippocampal ERK and p38MAPK Signaling in Neuropathic Pain Rats.

Wang JY, Chen SP, Gao YH, Qiao LN, Zhang JL, Liu JL - Evid Based Complement Alternat Med (2015)

Effect of EA on expression levels of hippocampal MEK, p-MEK proteins in different groups. Data are presented as mean ± SD (∗P < 0.05, compared with the sham control group; n = 5 in each group). (a) Upper panel shows representative immunoblots of MEK protein in the 5 groups: (1) sham control group, (2) CCI group, (3) CCI + EA2D group, (4) CCI + EA1W group, and (5) CCI + EA2W group; lower histograms show the relative expression levels of MEK protein in the 5 groups. (b) The lower histograms show the relative expression levels of p-MEK1 and p-MEK2 proteins in the five groups; upper panel shows the representative immunoblots of MEK1/2 proteins and GAPDH in different groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4487344&req=5

fig3: Effect of EA on expression levels of hippocampal MEK, p-MEK proteins in different groups. Data are presented as mean ± SD (∗P < 0.05, compared with the sham control group; n = 5 in each group). (a) Upper panel shows representative immunoblots of MEK protein in the 5 groups: (1) sham control group, (2) CCI group, (3) CCI + EA2D group, (4) CCI + EA1W group, and (5) CCI + EA2W group; lower histograms show the relative expression levels of MEK protein in the 5 groups. (b) The lower histograms show the relative expression levels of p-MEK1 and p-MEK2 proteins in the five groups; upper panel shows the representative immunoblots of MEK1/2 proteins and GAPDH in different groups.
Mentions: MEK1/2 (MKK1/2) are the upstream kinases of ERK signaling. Compared with the control group, the expression levels of hippocampal MEK and p-MEK1 proteins had no significant changes in the CCI, CCI + EA2D, CCI + EA1W, and CCI + EA2W groups (P > 0.05, Figure 3(a)), while that of p-MEK2 protein was significantly downregulated after CCI (P < 0.05, Figure 3(b)). Following EAS of ST36-GB34, p-MEK2 expression had a slight upregulation in the three EAS groups (P > 0.05) without significant differences among the three groups (P > 0.05).

Bottom Line: After CCI, the thermal pain thresholds of the affected hind were significantly decreased compared with the control group (P < 0.05).Following one and two weeks' EAS of ST 36-GB34, the pain thresholds were significantly upregulated (P < 0.05), and the effect of EA2W was remarkably superior to that of EA2D and EA1W (P < 0.05).The above mentioned results indicated that EA2W induced cumulative analgesic effect may be closely associated with its function in removing neuropathic pain induced suppression of intracellular ERK and p38MAPK signaling in the hippocampus.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Beijing 100700, China.

ABSTRACT
Results of our past studies showed that hippocampal muscarinic acetylcholine receptor (mAChR)-1 mRNA and differentially expressed proteins participating in MAPK signaling were involved in electroacupuncture (EA) induced cumulative analgesia in neuropathic pain rats, but the underlying intracellular mechanism remains unknown. The present study was designed to observe the effect of EA stimulation (EAS) on hippocampal extracellular signal-regulated kinases (ERK) and p38 MAPK signaling in rats with chronic constrictive injury (CCI) of the sciatic nerve, so as to reveal its related intracellular targets in pain relief. After CCI, the thermal pain thresholds of the affected hind were significantly decreased compared with the control group (P < 0.05). Following one and two weeks' EAS of ST 36-GB34, the pain thresholds were significantly upregulated (P < 0.05), and the effect of EA2W was remarkably superior to that of EA2D and EA1W (P < 0.05). Correspondingly, CCI-induced decreased expression levels of Ras, c-Raf, ERK1 and p-ERK1/2 proteins, and p38 MAPK mRNA and p-p38MAPK protein in the hippocampus tissues were reversed by EA2W (P < 0.05). The above mentioned results indicated that EA2W induced cumulative analgesic effect may be closely associated with its function in removing neuropathic pain induced suppression of intracellular ERK and p38MAPK signaling in the hippocampus.

No MeSH data available.


Related in: MedlinePlus