蒙浩洋, 李少军, 唐方萍, 黄艳妮, 罗海兰, 陈静雯, 邓祥发, 姜岳明. 对氨基水杨酸钠对亚慢性染锰大鼠基底前脑胆碱能神经细胞的影响[J]. 环境与职业医学, 2013, 30(6): 461-464.
引用本文: 蒙浩洋, 李少军, 唐方萍, 黄艳妮, 罗海兰, 陈静雯, 邓祥发, 姜岳明. 对氨基水杨酸钠对亚慢性染锰大鼠基底前脑胆碱能神经细胞的影响[J]. 环境与职业医学, 2013, 30(6): 461-464.
MENG Hao-yang , LI Shao-jun , TANG Fang-ping , HUANG Yan-ni , LUO Hai-lan , CHEN Jing-wen , DENG Xiang-fa , JIANG Yue-ming . Effects of Sodium Aminosalicylate on Basal Forebrain Choline Acetyltransferase Neurons of Rats Induced by Sub-Chronic Manganese Exposure[J]. Journal of Environmental and Occupational Medicine, 2013, 30(6): 461-464.
Citation: MENG Hao-yang , LI Shao-jun , TANG Fang-ping , HUANG Yan-ni , LUO Hai-lan , CHEN Jing-wen , DENG Xiang-fa , JIANG Yue-ming . Effects of Sodium Aminosalicylate on Basal Forebrain Choline Acetyltransferase Neurons of Rats Induced by Sub-Chronic Manganese Exposure[J]. Journal of Environmental and Occupational Medicine, 2013, 30(6): 461-464.

对氨基水杨酸钠对亚慢性染锰大鼠基底前脑胆碱能神经细胞的影响

Effects of Sodium Aminosalicylate on Basal Forebrain Choline Acetyltransferase Neurons of Rats Induced by Sub-Chronic Manganese Exposure

  • 摘要: 目的 探讨对氨基水杨酸钠(PAS-Na)对亚慢性染锰大鼠基底前脑胆碱能神经细胞的影响。

    方法 48只雄性SD大鼠被随机分为对照Ⅰ、Ⅱ组, 染锰Ⅰ、Ⅱ组, PAS-Na 预防(预防)组, PAS-Na 治疗(治疗)组, 每组8 只。染锰组、预防组、治疗组大鼠每日腹腔注射氯化锰(MnCl2O& #183;4H2O 15 mg/kg), 每周5 d, 对照组腹腔注射等容量生理盐水, 预防组在染锰同时每日背部皮下注射PAS-Na(200 mg/kg), 连续12 周。13 周开始, 治疗组每日背部皮下注射 PAS-Na(200 mg/kg), 同时染锰Ⅱ组、对照Ⅱ组背部皮下注射等容量生理盐水至18 周。采用水迷宫实验检测大鼠学习记忆能力, 免疫组化染色观察胆碱乙酰转移酶(ChAT)阳性神经元形态及数量, 检测基底前脑ChAT 蛋白活性。

    结果 12 周后, 染锰组逃避潜伏期、游泳路程均比对照Ⅰ组长, 预防组逃避潜伏期、游泳路程均较染锰组短(P < 0.05)。染锰组基底前脑垂直支臂核(vDB)/水平支臂核(hDB)ChAT 阳性细胞数较对照Ⅰ组少, 预防组vDB/hDB ChAT 阳性细胞数较染锰组多(P < 0.05); 染锰组大鼠基底前脑组织ChAT 蛋白活性较对照Ⅰ组低, 预防组较之回升(P < 0.05)。18 周后, 染锰组逃避潜伏期、游泳路程都比对照组长, 治疗组逃避潜伏期、游泳路程比染锰组短(P < 0.05)。染锰组vDB/hDB ChAT阳性细胞数较对照组少, 治疗组vDB ChAT 阳性细胞数较染锰Ⅱ组多(P < 0.05)。

    结论 PAS-Na 对亚慢性染锰引起大鼠基底前脑ChAT 阳性细胞减少、ChAT 蛋白活性降低和学习记忆障碍可能有拮抗作用。

     

    Abstract: Objective To explore the effects of sodium aminosalicylate (PAS-Na) on basal forebrain choline acetyltransferase (ChAT) neurons of rats induced by sub-chronic Mn exposure.

    Methods Forty-eight male SD rats were randomly assigned into 6 groups: control group I and Ⅱ, Mn-exposed group I and Ⅱ, PAS-Na prevention (PAS-P) group, and PAS-Na treatment (PAS-T) group, 8 rats for each group. The Mn-exposed group, the PAS-P group, and the PAS-T group received intraperitoneal injection (ip) of MnCl2O& #183;4H2O 15 mg/kg, the control group received ip of physiological saline at the same dose, and the PAS-P group received back subcutaneous injection (sc) of PAS-Na 200 mg/kg, all procedures were performed 5 days a week for 12 weeks. Then, the rats in the PAS-T group received back sc of PAS-Na 200 mg/kg, while the rats in the Mn-exposed group II and the control group II received back sc of physiological saline at the same volume once a day, for 6 weeks. Morris water maze was utilized to probe rats learning and memory capacity. Morphological change and ChAT positive neuron count in basal forebrain were recorded under microscope after immunohistochemistry staining, and ChAT protein activity was also detected.

    Results After 12 weeks, the escape latency and the swimming distance obviously increased in the Mn-exposed group I when compared with those of the control group I, but the treatment in the PAS-P group reversed the escape latency and swimming distance induced by Mn exposure (P < 0.05). The ChAT positive neuron count of basal forebrain vertical limb of diagonal band (vDB)/horizontal limb of diagonal band (hDB) and ChAT protein activity in the Mn-exposed group I were lower than those in the control group I, the treatment in the PAS-P group reversed distinctly vDB/hDB ChAT positive count and ChAT protein activity induced by Mn (P < 0.05). After 18 weeks, the escape latency and the swimming distance obviously increased in the Mn-exposed group Ⅱ when compared with those of the control group Ⅱ , but the treatment in the PAS-T group reversed the escape latency and the swimming distance induced by Mn (P < 0.05). The ChAT positive neuron count of basal forebrain vDB/hDB in the Mn-exposed group Ⅱwas lower than that in the control group Ⅱ, the treatment of the PAS-T group reversed distinctly vDB ChAT positive count induced by Mn (P < 0.05).

    Conclusion PAS-Na may reverse the number of ChAT positive neurons and ChAT protein activity reduced by manganese exposure. Therefore, it may have an interventive effect on learning capacity and memory impairment by manganese exposure.

     

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