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Hyperbaric oxygen treatment at various stages following chronic constriction injury produces different antinociceptive effects via regulation of P2X4R expression and apoptosis.

Zhao BS, Song XR, Hu PY, Meng LX, Tan YH, She YJ, Ding YY - PLoS ONE (2015)

Bottom Line: In addition, late HBO treatment reduced CCI-induced ultrastructural damage.HBO treatment at various stages following CCI can produce antinociceptive effects via different mechanisms.Early HBO treatment is associated with inhibition of P2X4R expression, and late HBO treatment is associated with inhibition of cell apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Guangzhou Women and Children's Medical Center, 510623, Guangzhou, China.

ABSTRACT

Purpose: The aims of this study were to investigate the effect of hyperbaric oxygen (HBO) treatment at various stages following chronic constriction injury (CCI) and to explore the underlying mechanisms of HBO treatment.

Methods: Forty adult male Sprague-Dawley rats were randomly assigned to five groups (n = 8 for each group): the sham group, CCI group, HBO1 group, HBO2 group, and HBO3 group. Neuropathic pain was induced by CCI of the sciatic nerve. HBO treatment began on postoperative days 1, 6, and 11 and continued for 5 days. The mechanical withdrawal threshold and thermal withdrawal latency were tested on preoperative day 3 and postoperative days 1, 3, 5, 7, 10, 14, and 21. The expression of P2X4R was determined by immunohistochemistry and western blot analysis. Cell apoptosis was measured using TUNEL staining. The expression of caspase 3 was measured using reverse transcription polymerase chain reaction (RT-PCR). Electron microscopy was used to determine the ultrastructural changes.

Results: Early HBO treatment beginning on postoperative day 1 produced a persistent antinociceptive effect and inhibited the CCI-induced increase in the expression of P2X4R without changing CCI-induced apoptosis. In contrast, late HBO treatment beginning on postoperative day 11 produced a persistent antinociceptive effect and inhibited CCI-induced apoptosis and upregulation of caspase-3 without changing the expression of P2X4R. In addition, late HBO treatment reduced CCI-induced ultrastructural damage. However, HBO treatment beginning on postoperative day 6 produced a transient antinociceptive effect without changing the expression of P2X4R or CCI-induced apoptosis.

Conclusion: HBO treatment at various stages following CCI can produce antinociceptive effects via different mechanisms. Early HBO treatment is associated with inhibition of P2X4R expression, and late HBO treatment is associated with inhibition of cell apoptosis.

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RT-PCR results showing the expression of caspase 3 on postoperative day 21 in the sham, CCI, HBO1, HBO2, and HBO3 groups.#p < 0.05 vs. sham, *p < 0.05 vs. CCI.
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pone.0120122.g004: RT-PCR results showing the expression of caspase 3 on postoperative day 21 in the sham, CCI, HBO1, HBO2, and HBO3 groups.#p < 0.05 vs. sham, *p < 0.05 vs. CCI.

Mentions: On postoperative day 7, compared with the sham group, the number of apoptotic cells was significantly increased by approximately 7-fold in the CCI group (Fig. 3A, B, G). Cell apoptosis declined at 10 days after CCI and remained higher than the control level on postoperative day 21 (Fig. 3A-G). On postoperative days 7 and 11, early and middleHBO treatment (HBO1 and HBO2 groups) did not prevent CCI-induced cell apoptosis (p > 0.05, Fig. 3A-D, G). However, on postoperative day 21, late HBO treatment beginning on postoperative day 11, but not early and middle HBO treatment, significantly inhibited CCI-induced cell apoptosis by approximately 2-fold (p < 0.05, Fig. 3E-G). In addition, late HBO treatment, but not early or middle HBO treatment, significantly inhibited the CCI-induced increase in the expression of caspase 3 (Fig. 4).


Hyperbaric oxygen treatment at various stages following chronic constriction injury produces different antinociceptive effects via regulation of P2X4R expression and apoptosis.

Zhao BS, Song XR, Hu PY, Meng LX, Tan YH, She YJ, Ding YY - PLoS ONE (2015)

RT-PCR results showing the expression of caspase 3 on postoperative day 21 in the sham, CCI, HBO1, HBO2, and HBO3 groups.#p < 0.05 vs. sham, *p < 0.05 vs. CCI.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4366063&req=5

pone.0120122.g004: RT-PCR results showing the expression of caspase 3 on postoperative day 21 in the sham, CCI, HBO1, HBO2, and HBO3 groups.#p < 0.05 vs. sham, *p < 0.05 vs. CCI.
Mentions: On postoperative day 7, compared with the sham group, the number of apoptotic cells was significantly increased by approximately 7-fold in the CCI group (Fig. 3A, B, G). Cell apoptosis declined at 10 days after CCI and remained higher than the control level on postoperative day 21 (Fig. 3A-G). On postoperative days 7 and 11, early and middleHBO treatment (HBO1 and HBO2 groups) did not prevent CCI-induced cell apoptosis (p > 0.05, Fig. 3A-D, G). However, on postoperative day 21, late HBO treatment beginning on postoperative day 11, but not early and middle HBO treatment, significantly inhibited CCI-induced cell apoptosis by approximately 2-fold (p < 0.05, Fig. 3E-G). In addition, late HBO treatment, but not early or middle HBO treatment, significantly inhibited the CCI-induced increase in the expression of caspase 3 (Fig. 4).

Bottom Line: In addition, late HBO treatment reduced CCI-induced ultrastructural damage.HBO treatment at various stages following CCI can produce antinociceptive effects via different mechanisms.Early HBO treatment is associated with inhibition of P2X4R expression, and late HBO treatment is associated with inhibition of cell apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Guangzhou Women and Children's Medical Center, 510623, Guangzhou, China.

ABSTRACT

Purpose: The aims of this study were to investigate the effect of hyperbaric oxygen (HBO) treatment at various stages following chronic constriction injury (CCI) and to explore the underlying mechanisms of HBO treatment.

Methods: Forty adult male Sprague-Dawley rats were randomly assigned to five groups (n = 8 for each group): the sham group, CCI group, HBO1 group, HBO2 group, and HBO3 group. Neuropathic pain was induced by CCI of the sciatic nerve. HBO treatment began on postoperative days 1, 6, and 11 and continued for 5 days. The mechanical withdrawal threshold and thermal withdrawal latency were tested on preoperative day 3 and postoperative days 1, 3, 5, 7, 10, 14, and 21. The expression of P2X4R was determined by immunohistochemistry and western blot analysis. Cell apoptosis was measured using TUNEL staining. The expression of caspase 3 was measured using reverse transcription polymerase chain reaction (RT-PCR). Electron microscopy was used to determine the ultrastructural changes.

Results: Early HBO treatment beginning on postoperative day 1 produced a persistent antinociceptive effect and inhibited the CCI-induced increase in the expression of P2X4R without changing CCI-induced apoptosis. In contrast, late HBO treatment beginning on postoperative day 11 produced a persistent antinociceptive effect and inhibited CCI-induced apoptosis and upregulation of caspase-3 without changing the expression of P2X4R. In addition, late HBO treatment reduced CCI-induced ultrastructural damage. However, HBO treatment beginning on postoperative day 6 produced a transient antinociceptive effect without changing the expression of P2X4R or CCI-induced apoptosis.

Conclusion: HBO treatment at various stages following CCI can produce antinociceptive effects via different mechanisms. Early HBO treatment is associated with inhibition of P2X4R expression, and late HBO treatment is associated with inhibition of cell apoptosis.

Show MeSH
Related in: MedlinePlus