褪黑素对噪声应激大鼠肝损伤的保护作用及其机制

Protective effects of melatonin on acute liver injury in rats induced by noise stress and its mechanism

目的:探讨褪黑素(MT)对噪声应激大鼠肝损伤的保护作用及可能机制.方法:将40只雄性SD大鼠随机分为5组:空白对照组、模型1组、模型2组、实验1组、实验2组,每组8只.实验组和模型组分别在应激前30min腹腔注射MT(15mg/kg)和等体积生理盐水.以56式冲锋枪射击时产生的120dB(A)的脉冲噪声,对实验组及模型组大鼠进行连续噪声刺激.噪声应激后,观察MT对各组大鼠血浆中皮质醇、超氧化物歧化酶(SOD),丙二醛(MDA)以及肝组织匀浆中SOD,MDA的影响.结果:肝脏病理检查显示模型组大鼠出现明显的病理性损伤,实验组大鼠损伤程度明显减轻;模型组大鼠血浆皮质醇、血浆及肝组织匀浆的MDA浓度较空白对照组显著升高,血浆及肝组织匀浆SOD活性显著降低(P<0.01),实验组大鼠血浆皮质醇的浓度、血浆及肝组织匀浆的MDA浓度较模型组显著降低,血浆及肝组织匀浆SOD活性显著升高(P<0.01).结论:MT能减轻噪声引起的大鼠肝损伤,其机制可能与抑制脂质过氧化反应有关.

AIM： To study the protective effects of melatonin on rats with hepatic injury induced by noise stress and its possible mechanism. METHODS： Forty SD rats were randomly divided into blank control group, experimental group and model group. Melatonin （ 15 mg/kg） and same volume of normal saline were given via intraperitoneal injection respectively to experimental group and model group 30 min before the noise stress. Both experimental group and model group were stimulated separately by 120 dB （A） impulse noise of type 56 submachine guns. After noise stress, the levels of cortisol, superoxide dismutase （SOD） , malondialdehyde （MDA） in blood plasma and SOD, MDA in homogenate of hepatic tissue were detected, and the structure of hepatic tissue was observed pathologically. RESULTS： Obvious hepatic pathological changes were observed in the model group, and that in experimental group were alleviated significantly. Compared to blank control group, levels of cortisol in blood plasma and levels of MDA in both liver and blood plasma in model group increased remarkably （P 〈0.01 ） and activity of SOD in both liver and blood plasma decreased greatly （ P 〈 0.01 ）. Compared to model group, levels of cortisol in blood plasma and levels of MDA in both liver and blood plasma decreased significantly （P 〈 0.01 ） , and activity of SOD in both liver and blood plasma increased obviously in experimental group. CONCLUSION： Melatonin alleviate the hepatic injury caused by noise stress. The mechanism may involve its role in inhibition of lipid peroxidation.