虾青素对慢性有机磷中毒小鼠神经的保护作用

NEUROPROTECTIVE EFFECT OF ASTAXANTHIN ON CHRONIC ORGANOPHOSPHATE POISONING MICE

目的探讨虾青素(AST)对慢性有机磷中毒小鼠神经的保护作用。方法成年健康雄性昆明种小鼠30只,随机选取8只小鼠作为对照组,其余22只小鼠连续氧乐果染毒4周建立慢性有机磷中毒模型,染毒结束后选取造模成功的16只小鼠随机分为模型组8只,AST组8只。AST组用花生油将AST稀释至浓度为1g/L,每天按50mg/kg灌胃给药,连续4周。对照组和模型组同步灌胃给予等体积的花生油,连续4周。采用ELISA法检测各组小鼠脑组织中活性氧(ROS)的含量,采用化学比色法检测各组小鼠海马组织谷胱甘肽过氧化物酶(GSHPX)活性,采用苏木精-伊红(HE)染色观察各组小鼠海马组织形态学变化,采用原位末端标记(TUNEL)方法检测各组小鼠海马区神经细胞凋亡情况。结果模型组小鼠慢性有机磷中毒后,脑组织ROS含量较对照组明显升高(F=144.60,q=24.05,P<0.05);GSH-PX活性较对照组显著降低(F=141.70,q=23.77,P<0.05);海马区神经元损伤明显,神经细胞凋亡数量较对照组显著增多(F=74.58,q=17.20,P<0.05)。AST组ROS含量较模型组明显降低(q=11.78,P<0.05);GSH-PX活性显著升高(q=10.70,P<0.05);海马区神经元损伤减轻,神经细胞凋亡数量较模型组明显降低(q=9.94,P<0.05)。结论 AST通过发挥其抗氧化、抑制细胞凋亡作用,对慢性有机磷中毒小鼠起到神经保护作用。

Objective To investigate the neuroprotective effect of astaxanthin（AST）on chronic organophosphate poisoning（COP）mice Methods This study consisted of 30 adult healthy male Kunming mice.Adopting random number table method,eight mice were selected to serve as control group,and the other 22 mice were used to create a COP model with subcutaneous injection of Omethoate（5mg/kg）,once a day,for four weeks.After the models were completed,16 successful mouse models were selected and equally divided into model group and AST group in random.In AST group,AST was diluted with peanut oil to a concentration of 1g/L,and 50mg/kg,by gavage,once a day,was given to the mice for four weeks.Mice in the control and model groups were given equal volume of peanut oil by gavage for four weeks.Content of ROS in brain tissue of mice in each group was measured using enzyme-linked immunosorbent assay（ELISA）,activity of glutathione peroxidase（GSH-PX）in hippocampus was assessed applying chemical colorimetry,morphology of hippocampus was observed by HE staining and apoptotic cells were counted employing terminal deoxynucleotidyl transferase dUTP nick end labeling assay（TUNEL）. Results Compared with the control group,after COP,the content of ROS in brain tissue of mice in the model group was obviously higher（F=144.60,q=24.05,P〈0.05）,the activity of GSH-PX was apparently lower（F=141.70,q=23.77,P〈0.05）,the hippocampus neuronal injury was more obvious and the number of neuronal apoptosis was much increased（F=74.58,q=17.20,P〈0.05）.Compared with the model group,the ROS content in the AST group obviously declined（q=11.78,P〈0.05）,the activity of GSH-PX significantly elevated（q=10.70,P〈0.05）,neuronal damage and the number of apoptotic cells markedly reduced（q=9.94,P〈0.05）. Conclusion AST exerts its antioxidant activity and inhibits apoptosis playing a neuroprotective role for chronic omethoate poisoning mice.