CAJ | 학술논문

目的探讨大蒜油对2,5-己二酮(2,5-hexanedione,2,5-HD)导致的大鼠神经组织氧化损伤的拮抗作用和对周围运动神经毒性的影响.方法 Wistar雄性大鼠40只,随机分为正常对照组、模型组、人蒜油低、高剂量组,每组10只.模型组及大蒜油低、高剂量组分别给予2,5-HD 300ms/ks腹腔注射,正常对照组给予生理盐水,5次/周,持续6周.大蒜油低、高剂量组提前1周分别给予40和80mg/kg大蒜油灌胃,持续至实验结束.测定后肢撑力指数和平衡指数等神经行为学指标,实验结束取脑、脊髓和坐骨神经分别测定丙二醛(MDA)、还原型谷胱廿肽(CSH)含量、总抗氧化能力(T-AOC)和抑制羟自由基能力.结果与第0周比较,后肢撑力指数第4周模型组升高44%,大蒜油低剂量组升高50%,大蒜油高剂量组升高49%,但3组间差异无统计学意义(P>0.05);第4周模型组平衡指数降低30%,大蒜油低剂量组降低45%,大蒜油高剂量组降低68%,与模型组相比,差异有统计学意义(P<0.01).大蒜油低、高剂基组大鼠在第4周即出现运动异常,较模型组人鼠提前1周;各组步态评分,模型组,大蒜油低、高剂量组均明显高于对照组,且大蒜油高剂量组高于模型组,差异均有统计学意义(P<0.05).在大脑、脊髓和坐骨神经中,与正常对照组相比,模型组人鼠MDA含量升高,抑制羟自由基能力降低,差异均有统计学意义(P<0.05或P<0.01);与模型组比较,大蒜油低、高剂量组在各神经组织中MDA含量均明显降低,抑制羟自由基能力明显升高,差异均有统计学意义(P<0.01).结论大蒜油可拮抗2,5-HD所致的大鼠神经组织氧化损伤,但并末改善2,5-HD导致的周围运动神经损伤,提示氧化-抗氧化损伤不是2,5-HD中毒性神经病的主要机制.
목적 탐토대산유대2,5-기이동(2,5-hexanedione,2,5-HD)도치적대서신경조직양화손상적길항작용화대주위운동신경독성적영향.방법 Wistar웅성대서40지,수궤분위정상대조조、모형조、인산유저、고제량조,매조10지.모형조급대산유저、고제량조분별급여2,5-HD 300ms/ks복강주사,정상대조조급여생리염수,5차/주,지속6주.대산유저、고제량조제전1주분별급여40화80mg/kg대산유관위,지속지실험결속.측정후지탱력지수화평형지수등신경행위학지표,실험결속취뇌、척수화좌골신경분별측정병이철(MDA)、환원형곡광입태(CSH)함량、총항양화능력(T-AOC)화억제간자유기능력.결과 여제0주비교,후지탱력지수제4주모형조승고44%,대산유저제량조승고50%,대산유고제량조승고49%,단3조간차이무통계학의의(P>0.05);제4주모형조평형지수강저30%,대산유저제량조강저45%,대산유고제량조강저68%,여모형조상비,차이유통계학의의(P<0.01).대산유저、고제기조대서재제4주즉출현운동이상,교모형조인서제전1주;각조보태평분,모형조,대산유저、고제량조균명현고우대조조,차대산유고제량조고우모형조,차이균유통계학의의(P<0.05).재대뇌、척수화좌골신경중,여정상대조조상비,모형조인서MDA함량승고,억제간자유기능력강저,차이균유통계학의의(P<0.05혹P<0.01);여모형조비교,대산유저、고제량조재각신경조직중MDA함량균명현강저,억제간자유기능력명현승고,차이균유통계학의의(P<0.01).결론 대산유가길항2,5-HD소치적대서신경조직양화손상,단병말개선2,5-HD도치적주위운동신경손상,제시양화-항양화손상불시2,5-HD중독성신경병적주요궤제.
Objective To investigate the effects of garlic oil(GO) against the peroxidation damage of rat nerve tissue and the peripheral motor neuropathy induced by 2,5-HD. Methods Male Wis Wistar rats were divided into four groups, with 10 in each group. The model group, and low and high doses of GO groups were administrated with 2,5-HD (ip, 300 mg/kg), respectively; The control group was treated with sodium chloride, five times per week for six weeks. Pretreatment with GO garaged (40 mg/kg or 80 mg/kg) started one week before 2,5-HD treatment, and lasted to the end of the experiment. Neurobehavioral indexes were examined at the zero,second and fourth week. At the end of the experiment,the scores of the gait,and the concentration of MDA and GSH, the level of T-AOC and the ability of inhibition of" OH in cerebrum, spinal cord and sciatic nerve were examined. Results Compared with the zero week, except of the control group rats, the hind limb landing foot splays of three groups rats decreased by 44%, 50% and 49% at the fourth week, respectively without significant difference. The threshold value of balance in model,GO low and high doses groups rats decreased by 30%, 45% and 68% at the fourth week, respectively, and lower than the control group rats(P<0.01 ).GO low and high doses groups rats showed the serious abnormity at the fourth week, before one week of the model group rats. The scores of gait of model,and GO low and high doses groups rats increased significantly compared with control group rats, and the GO high dose group rats were higher than model group rats(P<0.05 ).by 2,5-HD in cerebrum,spinal cord and sciatic nerve. The concentration of MDA increased,and the level of spinal cord and sciatic nerve increased, the concentration of MDA of GO low doses group rats decreased, the creased( P<0.01 )respectively, and the level of the ability of inhibition of" OH increased (P<0.01) in nerve tissue. Conclusion GO has antagonist effect on the 2,5-HD induced peroxidation damage, but can not improve the function of the peripheral motor nerve, indicating that the lipid peroxidation does not play an important role in 2,5-HD neurotoxieity.