本文關鍵詞： 對氨基水楊酸鈉 錳 氨基酸類神經遞質 鐵蛋白 轉鐵蛋白　出處：《廣西醫(yī)科大學》2012年碩士論文　論文類型：學位論文

【摘要】：[目的]探討PAS-Na對錳致大鼠丘腦和基底節(jié)氨基酸類神經遞質水平和鐵代謝的影響。[方法]130只雄性SD大鼠按完全隨機法分為染錳組、PAS-Na預防性干預組(P-PAS組)、低劑量PAS-Na (L-PAS)治療組、中劑量PAS-Na (M-PAS)治療組、高劑量PAS-Na (H-PAS)治療組和正常對照(對照組),觀察期為4周(染錳4周)、8周(染錳+PAS預防8周)、12周(染錳+PAS預防12周)、18周(染錳12周+治療6周)。給染錳、預防、L-、M-和H-PAS治療組腹腔注射MnCl2·4H2O15mg/kg,對照組腹腔注射等容量生理鹽水,每日1次,每周5d,連續(xù)4周、8周或12周。P-PAS組染錳的同時背部皮下注射PAS-Na200mg/kg,每周3次,連續(xù)8周或12周。然后,給L-、M-和H-PAS治療組背部皮下注射PAS-Na100、200或300mg/kg,其余組背部皮下注射等容量生理鹽水,每日1次,連續(xù)6周。每周測量一次體重。用HPLC熒光檢測法測定丘腦中Glu、Gln、Gly、GABA含量；用ELISA試劑盒測定丘腦和基底核中鐵蛋白、轉鐵蛋白含量。[結果]觀察期2、3、4、5、8、11周時,染錳組體重都低于對照組(P0.05),P-PAS組體重均高于染錳組,但無顯著性差異(P0.05)；觀察期18周時,染錳組體重在停止染錳后逐漸恢復至對照組水平,各治療組大鼠經PAS-Na治療后體重增長速度逐漸恢復最后接近對照組水平,但各組體重無顯著性差異(P0.05)。觀察期4、8、12周時,各組大鼠丘腦Glu、Gln、Gly、GABA含量無明顯差異(P0.05)。觀察期18周時,染錳組Glu水平明顯低于對照組,L-PAS治療組Glu含量明顯高于染錳組(P0.05)。觀察期4、8、12周時各組丘腦鐵蛋白和轉鐵蛋白含量無顯著性差異(P0.05)。觀察期18周時,染錳組轉鐵蛋白含量高于對照組(P0.05),各治療組轉鐵蛋白含量較染錳組下降(P0.05),且高PAS治療組較其余兩個劑量治療組下降明顯。在基底節(jié),觀察期4、8、12周時各組鐵蛋白和轉鐵蛋白含量無明顯差異。觀察期18周時,L-PAS治療組轉鐵蛋白含量明顯低于染錳組(P0.05)。[結論]1.染錳會降低大鼠體重增長速度；2.錳對大鼠丘腦Glu和Gln的損害呈持續(xù)性,PAS-Na對染錳大鼠Glu含量的有害影響可能有一定的拮抗作用。3. PAS-Na治療可能使染錳大鼠丘腦和基底神經節(jié)轉鐵蛋白含量減少。
[Abstract]:[Objective] to investigate the effect of PAS-Na on the level of amino acid neurotransmitters and iron metabolism in rat thalamus and basal ganglia. [Methods: 130 male Sprague-Dawley rats were randomly divided into two groups: PAS-Na preventive intervention group and low-dose PAS-Na L-PAS-treated group. Middle dose PAS-Na M-PAS-treated group, high-dose PAS-Na H-PAS-treated group and normal control group (control group, the observation period was 4 weeks (manganese exposure 4 weeks). 8 weeks (8 weeks after exposure to manganese PAS) and 12 weeks after exposure to manganese PAS (12 weeks after exposure to manganese PAS) and 18 weeks after treatment (12 weeks of manganese exposure and 6 weeks of treatment). M- and H-PAS treatment group were intraperitoneally injected with MnCl2 路4H2O 15mg / kg, while the control group was intraperitoneally injected with normal saline of the same volume, once a day, 5 days a week for 4 weeks. PAS-Na 200 mg / kg was injected subcutaneously into the back of the group of 8 or 12 weeks. Then, L- was given to L-, three times a week for 8 or 12 weeks. In the M- and H-PAS treatment group, PAS-Na 100 mg / kg was injected subcutaneously into the back of the rats, and the rest group was subcutaneously injected with the same volume of normal saline once a day. The body weight was measured once a week for 6 weeks. The content of Glun Gln GlyGABAs in the thalamus was determined by HPLC fluorescence assay. The contents of ferritin and transferrin in thalamus and basal nucleus were determined by ELISA kit. [Results: at 11 weeks after observation, the body weight of the manganese exposed group was lower than that of the control group (P 0.05) and P-PAS group was higher than that of the manganese group, but there was no significant difference (P 0.05). After 18 weeks of observation, the weight of the manganese exposed group gradually recovered to the level of the control group after stopping the exposure to manganese, and the weight growth rate of the rats in each treatment group gradually recovered to the level of the control group after PAS-Na treatment. However, there was no significant difference in body weight in each group (P 0.05). There was no significant difference in GABA content between the two groups. At 18 weeks of observation, the level of Glu in the manganese exposed group was significantly lower than that in the control group. The content of Glu in L-PAS treatment group was significantly higher than that in manganese exposed group (P 0.05). There was no significant difference in the levels of thalamic ferritin and transferrin in each group at 12 weeks. At 18 weeks after observation, the transferrin content in manganese exposed group was higher than that in control group (P 0.05). The levels of transferrin in each treatment group were significantly lower than those in the manganese exposed group, and the levels of transferrin in the high PAS group were significantly lower than those in the other two dose groups. There was no significant difference in the levels of ferritin and transferrin in each group at 12 weeks, but the transferrin content in L-PAS treatment group was significantly lower than that in manganese exposed group at 18 weeks. [Conclusion: 1. Manganese exposure can decrease the weight growth rate of rats; 2. The damage of manganese to Glu and Gln in rat thalamus was sustained. The harmful effect of PAS-Na on Glu content in manganese exposed rats may have some antagonistic effect. 3. The level of transferrin in thalamus and basal ganglion of rats exposed to manganese may be decreased by PAS-Na treatment.
【學位授予單位】：廣西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2012
【分類號】：R114

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