2015•Zhonghua mazuixue zazhiRequires access

Effect of hyperbaric oxygen on expression of fractalkine in nerve tissues of rats with neuropathic pain

Baisong Zhao, Yongying Pan

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Abstract

Objective To investigate the effect of hyperbaric oxygen on the expression of fractalkine (FKN) in the nerve tissues of rats with neuropathic pain (NP). Methods Thirty-two male Sprague-Dawley rats, weighing 250-280 g, aged 10-12 weeks, were divided into 4 groups (n= 8 each) using the random number table: control group (group C), sham operation group (group S), group NP, and hyperbaric oxygen group (group H). NP was induced by chronic constriction injury (CCI) in anesthetized rats. The left sciatic nerve was exposed, and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread. Group H received hyperbaric oxygen therapy once a day for 5 consecutive days starting from day 1 after CCI. The rats were placed into the hyperbaric oxygen chamber, which was pressurised to 2 atmosphere absolute at a rate of 10 kPa/min, and maintained at this level for 60 min. The pressure was then decreased to the normal pressure at a rate of 10 kPa/min. The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before CCI, and 3, 5, 7 and 14 days after CCI. After measurement of pain threshold at 3 and 7 days after CCI, 4 rats were selected and sacrificed. The sciatic nerve and lumbar segment of the spinal cord were removed for determination of the expression of FKN by Western blot. Results Compared with group C, the MWT was significantly decreased, and TWL was shortened at each time point after CCI, the expression of FKN in the sciatic nerve at 3 days after CCI, and in the sciatic nerve and spinal cord at 3 and 7 days after CCI was up-regulated in group NP (P 0.05). Compared with group NP, the MWT was significantly increased, and TWL was prolonged at each time point after CCI, and the expression of FKN in the sciatic nerve at 3 days after CCI, and in the sciatic nerve and spinal cord at 3 and 7 days after CCI was down-regulated in group H (P<0.05). Conclusion The mechanism by which hyperbaric oxygen mitigates NP is related to inhibition of over-expression of FKN in the nerve tissues of rats. Key words: Hyperbaric oxygenation; Neuralgia; Chemotactic factors

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Objective To investigate the effect of hyperbaric oxygen on the expression of fractalkine (FKN) in the nerve tissues of rats with neuropathic pain (NP). Methods Thirty-two male Sprague-Dawley rats, weighing 250-280 g, aged 10-12 weeks, were divided into 4 groups (n= 8 each) using the random number table: control group (group C), sham operation group (group S), group NP, and hyperbaric oxygen group (group H). NP was induced by chronic constriction injury (CCI) in anesthetized rats. The left sciatic nerve was exposed, and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread. Group H received hyperbaric oxygen therapy once a day for 5 consecutive days starting from day 1 after CCI. The rats were placed into the hyperbaric oxygen chamber, which was pressurised to 2 atmosphere absolute at a rate of 10 kPa/min, and maintained at this level for 60 min. The pressure was then decreased to the normal pressure at a rate of 10 kPa/min. The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before CCI, and 3, 5, 7 and 14 days after CCI. After measurement of pain threshold at 3 and 7 days after CCI, 4 rats were selected and sacrificed. The sciatic nerve and lumbar segment of the spinal cord were removed for determination of the expression of FKN by Western blot. Results Compared with group C, the MWT was significantly decreased, and TWL was shortened at each time point after CCI, the expression of FKN in the sciatic nerve at 3 days after CCI, and in the sciatic nerve and spinal cord at 3 and 7 days after CCI was up-regulated in group NP (P 0.05). Compared with group NP, the MWT was significantly increased, and TWL was prolonged at each time point after CCI, and the expression of FKN in the sciatic nerve at 3 days after CCI, and in the sciatic nerve and spinal cord at 3 and 7 days after CCI was down-regulated in group H (P<0.05). Conclusion The mechanism by which hyperbaric oxygen mitigates NP is related to inhibition of over-expression of FKN in the nerve tissues of rats. Key words: Hyperbaric oxygenation; Neuralgia; Chemotactic factors

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Available abstract

Objective To investigate the effect of hyperbaric oxygen on the expression of fractalkine (FKN) in the nerve tissues of rats with neuropathic pain (NP). Methods Thirty-two male Sprague-Dawley rats, weighing 250-280 g, aged 10-12 weeks, were divided into 4 groups (n= 8 each) using the random number table: control group (group C), sham operation group (group S), group NP, and hyperbaric oxygen group (group H). NP was induced by chronic constriction injury (CCI) in anesthetized rats. The left sciatic nerve was exposed, and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread. Group H received hyperbaric oxygen therapy once a day for 5 consecutive days starting from day 1 after CCI. The rats were placed into the hyperbaric oxygen chamber, which was pressurised to 2 atmosphere absolute at a rate of 10 kPa/min, and maintained at this level for 60 min. The pressure was then decreased to the normal pressure at a rate of 10 kPa/min. The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before CCI, and 3, 5, 7 and 14 days after CCI. After measurement of pain threshold at 3 and 7 days after CCI, 4 rats were selected and sacrificed. The sciatic nerve and lumbar segment of the spinal cord were removed for determination of the expression of FKN by Western blot. Results Compared with group C, the MWT was significantly decreased, and TWL was shortened at each time point after CCI, the expression of FKN in the sciatic nerve at 3 days after CCI, and in the sciatic nerve and spinal cord at 3 and 7 days after CCI was up-regulated in group NP (P 0.05). Compared with group NP, the MWT was significantly increased, and TWL was prolonged at each time point after CCI, and the expression of FKN in the sciatic nerve at 3 days after CCI, and in the sciatic nerve and spinal cord at 3 and 7 days after CCI was down-regulated in group H (P<0.05). Conclusion The mechanism by which hyperbaric oxygen mitigates NP is related to inhibition of over-expression of FKN in the nerve tissues of rats. Key words: Hyperbaric oxygenation; Neuralgia; Chemotactic factors

Key concepts: Neuropathic pain, Anesthesia, Sciatic nerve, Medicine, Hyperbaric oxygen, Lumbar, Spinal cord, Threshold of pain

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Effect of hyperbaric oxygen on expression of fractalkine in nerve tissues of rats with neuropathic pain — Research Paper | ScholarLens