中华精神科杂志
中華精神科雜誌
중화정신과잡지
CHINESE JOURNA OF PSYCHIATRY
2014年
5期
303-307
,共5页
李爽%李新娟%张艳%杜爱林%徐春阳%张瑞岭
李爽%李新娟%張豔%杜愛林%徐春暘%張瑞嶺
리상%리신연%장염%두애림%서춘양%장서령
酒精中毒%奎硫平%谷氨酸%受体,大麻酚,CB1
酒精中毒%奎硫平%穀氨痠%受體,大痳酚,CB1
주정중독%규류평%곡안산%수체,대마분,CB1
Alcoholism%Quetiapine%Glutamic acid%Receptor,cannabinoid,CB1
目的 分析奎硫平对慢性酒精中毒大鼠海马谷氨酸含量及大麻素受体1(CB1)表达的影响.方法 将48只大鼠按随机数字表法分为对照组、酒精中毒模型组、酒精中毒+低剂量奎硫平组、酒精中毒+高剂量奎硫平组,每组12只.建立大鼠慢性酒精中毒模型,采用戒断评分表检测各组大鼠戒断水平,高效液相色谱法检测海马组织中谷氨酸含量,实时定量PCR检测海马组织CB1mRNA含量,免疫荧光检测海马组织CB1蛋白表达.结果 酒精中毒模型组与对照组比较,戒断评分[(11.20±3.01)分与(5.50±1.90)分]、海马组织中谷氨酸含量[(0.26±0.06) μmol/g与(3.55 ±0.67) μmol/g]、CBl mRNA相对拷贝数(7.53±0.80与1.83 ±0.81),差异均有统计学意义(t=5.06、15.52、15.88,均P＜0.05);酒精中毒+高剂量奎硫平组与酒精中毒模型组比较,戒断评分[(6.70±1.34)分与(11.20±3.01)分]、海马组织中谷氨酸含量[(2.56±0.55) μmol/g与(0.26±0.06) μmol/g]、CBl mRNA相对拷贝数(1.95±0.65与7.53±0.80)差异均有统计学意义(t=4.32、13.19、17.11,均P＜0.05);酒精中毒模型组大鼠海马区CB1阳性细胞较对照组明显增加,给予高剂量奎硫平干预后CB1阳性细胞数量较酒精中毒模型组减少.结论 奎硫平可以减轻大鼠酒精戒断症状,其作用机制可能与内源性大麻素-CBl/谷氨酸通路调节有关.
目的 分析奎硫平對慢性酒精中毒大鼠海馬穀氨痠含量及大痳素受體1(CB1)錶達的影響.方法 將48隻大鼠按隨機數字錶法分為對照組、酒精中毒模型組、酒精中毒+低劑量奎硫平組、酒精中毒+高劑量奎硫平組,每組12隻.建立大鼠慢性酒精中毒模型,採用戒斷評分錶檢測各組大鼠戒斷水平,高效液相色譜法檢測海馬組織中穀氨痠含量,實時定量PCR檢測海馬組織CB1mRNA含量,免疫熒光檢測海馬組織CB1蛋白錶達.結果 酒精中毒模型組與對照組比較,戒斷評分[(11.20±3.01)分與(5.50±1.90)分]、海馬組織中穀氨痠含量[(0.26±0.06) μmol/g與(3.55 ±0.67) μmol/g]、CBl mRNA相對拷貝數(7.53±0.80與1.83 ±0.81),差異均有統計學意義(t=5.06、15.52、15.88,均P＜0.05);酒精中毒+高劑量奎硫平組與酒精中毒模型組比較,戒斷評分[(6.70±1.34)分與(11.20±3.01)分]、海馬組織中穀氨痠含量[(2.56±0.55) μmol/g與(0.26±0.06) μmol/g]、CBl mRNA相對拷貝數(1.95±0.65與7.53±0.80)差異均有統計學意義(t=4.32、13.19、17.11,均P＜0.05);酒精中毒模型組大鼠海馬區CB1暘性細胞較對照組明顯增加,給予高劑量奎硫平榦預後CB1暘性細胞數量較酒精中毒模型組減少.結論 奎硫平可以減輕大鼠酒精戒斷癥狀,其作用機製可能與內源性大痳素-CBl/穀氨痠通路調節有關.
목적 분석규류평대만성주정중독대서해마곡안산함량급대마소수체1(CB1)표체적영향.방법 장48지대서안수궤수자표법분위대조조、주정중독모형조、주정중독+저제량규류평조、주정중독+고제량규류평조,매조12지.건립대서만성주정중독모형,채용계단평분표검측각조대서계단수평,고효액상색보법검측해마조직중곡안산함량,실시정량PCR검측해마조직CB1mRNA함량,면역형광검측해마조직CB1단백표체.결과 주정중독모형조여대조조비교,계단평분[(11.20±3.01)분여(5.50±1.90)분]、해마조직중곡안산함량[(0.26±0.06) μmol/g여(3.55 ±0.67) μmol/g]、CBl mRNA상대고패수(7.53±0.80여1.83 ±0.81),차이균유통계학의의(t=5.06、15.52、15.88,균P＜0.05);주정중독+고제량규류평조여주정중독모형조비교,계단평분[(6.70±1.34)분여(11.20±3.01)분]、해마조직중곡안산함량[(2.56±0.55) μmol/g여(0.26±0.06) μmol/g]、CBl mRNA상대고패수(1.95±0.65여7.53±0.80)차이균유통계학의의(t=4.32、13.19、17.11,균P＜0.05);주정중독모형조대서해마구CB1양성세포교대조조명현증가,급여고제량규류평간예후CB1양성세포수량교주정중독모형조감소.결론 규류평가이감경대서주정계단증상,기작용궤제가능여내원성대마소-CBl/곡안산통로조절유관.
Objective To observe the effect of quetiapine on levels of glutamate and expression of cannabinoid receptor type 1 (CB1) in the hippocampus of rats with chronic alcoholism.Methods Fortyeight rats were randomly divided into 4 groups of 12:control group,chronic alcoholism group,low and high quetiapine groups (both with chronic alcoholism),to establish an animal model of chronic alcoholism.The abstinence scoring was used to evaluate the rats' withdrawal symptom; the concentrations of glutamate in rats' hippocampus were measured by high-performance liquid chromatography (HPLC) ; expression of CB1 mRNA was evaluated by real-time quantitative PCR,CB1 protein expression in the hippocampus was detected by immunofluorescence.Results The abstinence score (11.20 ± 3.01 vs.5.50 ± 1.90),glutamate content ((0.26 ± 0.06) μmol/g vs.(3.55 ± 0.67) μmol/g),CB1 mRNA relative copy numbers (7.53 ± 0.80 vs.1.83 ± 0.81) were significantly different in the chronic alcoholism group as compared to the control group (t =5.06,15.52,15.88,all P ＜ 0.05).The abstinence score (6.70 ± 1.34 vs.11.20 ± 3.01),glutamate content((2.56 ± 0.55) μmol/g vs.(0.26 ±0.06) μmoL/g),CB1 mRNA relative copy numbers (1.95 ± 0.65 vs.7.53 ± 0.80) were also significantly different in the high quetiapine group as compared to the chronic alcoholism group (t =4.32,13.19,17.11,all P ＜ 0.05) ; immunofluorescence showed that CB1 positive cells in the chronic alcoholism group were significantly increased compared with the control group,and CB1 positive cells in the high quetiapine group were significantly decreased compared with the chronic alcoholism group.Conclusion Quetiapine may alleviate the damage from chronic alcoholism,the mechanism may be relate to the regulation of the CB1/glutamate pathway.
