Abstract
Objective To evaluate the effect of ganglioside (GM-1) preconditioning on endoplasmic reticulum stress (ERS)-dependent apoptosis during spinal cord injury induced by bupivacaine in rats. Methods One hundred and eight clean-grade healthy male Sprague-Dawley rats, aged 8 weeks, weighing 250-300 g, were divided into 3 groups (n=36 each) using a random number table method: control group (group C), bupivacaine group (group B) and GM-1 pretreatment group (group G). In group B, 5% bupivacaine 0.12 μl/g was intrathecally injected at 1.5 h intervals, 3 times intotal.In group G, GM-1 20 μl (30 mg/kg) was intrathecally injected, and 24 h later bupivacaine was intrathecally injected according to the method previously described in group B. Immediately after intrathecal injection and at 1, 3, 5, 7 and 14 days after intrathecal injection, the maximum percentage of anti-nociceptive effects (%MPE) was detected, the hindlimb motor function score (BBB score) was evaluated, and spinal cord tissues were harvested for determination of cell apoptosis (using TUNEL) and expression of caspase-12 and CCAAT/enhancer-binding protein homologous protein(CHOP) protein and mRNA (by Western blot or quantitative real-time polymerase chain reaction). The apoptosis rate was calculated. Results Compared with group C, the %MPE and apoptosis rate were significantly increased, the BBB score was decreased, and the expression of CHOP and caspase-12 protein and mRNA was up-regulated in group B (P<0.05). Compared with group B, the %MPE and apoptosis rate were significantly decreased, the BBB score was increased, and the expression of CHOP and caspase-12 protein and mRNA was down-regulated in group G (P<0.05). Conclusion GM-1 preconditioning reduces bupivacaine-induced spinal cord injury possibly through inhibiting ERS-dependent apoptosis in rats. Key words: Ganglioside; Bupivacaine; Endoplasmic reticulum stress; Apoptosis
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