中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2012年
4期
385-388
,共4页
于佳男%魏灿%张鼎%裴俊瑞%李德安%周令望%冯红旗%孙树秋
于佳男%魏燦%張鼎%裴俊瑞%李德安%週令望%馮紅旂%孫樹鞦
우가남%위찬%장정%배준서%리덕안%주령망%풍홍기%손수추
硒%黄绿青霉素%蛋白质%心肌%生物化学
硒%黃綠青黴素%蛋白質%心肌%生物化學
서%황록청매소%단백질%심기%생물화학
Selenium%Citreoviridin%Proteins%Myocardium%Biochemistry
目的 观察黄绿青霉素(CIT)对低硒低蛋白大鼠心肌损伤在生化水平上的特点.方法 48只4周龄Wistar雄性大鼠,2×2析因设计,按体质量随机分为4组:低硒低蛋白加CIT组、低硒低蛋白组、常硒常蛋白加CIT组、常硒常蛋白组,每组12只.分别采用低硒低蛋白和常硒常蛋白饲料喂养大鼠至第12周后,加毒素组大鼠饲料中加入8mg·kg-1·d-1 CIT喂养至第20周,再加量至10 mg·kg-1·d-1 CIT继续喂养至22周,股动脉采血及取心脏,检测血清肌钙蛋白Ⅰ(Tn-Ⅰ)、白蛋白水平,肌酸激酶(CK)、谷胱甘肽过氧化物酶( GSH-Px)以及心肌超氧化物歧化酶(SOD)活性,总抗氧化能力(T-AOC).结果 “硒+蛋白”与CIT对大鼠终来体质量、白蛋白和Tn-Ⅰ存在交互作用(F值分别为8.186、6.160、19.183,P均＜0.05),对12周大鼠体质量,22周血清GSH-Px、CK水平以及心肌SOD、T-AOC活性的影响不存在交互作用(F值分别为1.633、1.987、0.075、0.474、1.145,P均＞ 0.05).在低硒低蛋白背景下,加CIT组血清白蛋白和Tn-Ⅰ水平[(42.88±1.19)g/L,(668.6±55.8) ng/L]均低于无CIT组[(47.59±1.05)g/L,(989.3±49.2)ng/L,P均＜0.05].“硒+蛋白”对12周大鼠体质量、22周血清GSH-Px活性以及心肌SOD、T-AOC有影响(F值分别为96.860、58.086、4.475、25.485,P均＜0.05).低硒低蛋白两组12周大鼠体质量[(186.33±7.89)、(197.83±7.89)g]均低于常硒常蛋白两组[(274.08±7.89)、(265.42±7.89)g,P均＜0.05]；低硒低蛋白两组[(317.5±102.6)、(296.9±90.5)U/L]血清GSH-Px活性均低于常硒常蛋白两组[(926.1±110.9)、(1181.7±85.9) U/L,P均＜0.05]；低硒低蛋白两组心肌SOD活性[ (65.22±5.91)×106、(62.68±5.61)× 106 U/kg]均低于常硒常蛋白两组[(74.07±7.24)×106、(80.07±5.91)×106 U/kg,P均＜0.05]；低硒低蛋白两组心肌T-AOC活性[(1.138±0.086)×106、(0.806±0.081)× 106U/kg]均低于常硒常蛋白两组[(1.688±0.105)×106、(1.163±0.086)×106 U/kg,P均＜0.05].结论 低硒低蛋白模型复制成功,CIT对低硒低蛋白大鼠心肌损伤在生化水平未发现有规律性效应,有待进一步研究确定.
目的 觀察黃綠青黴素(CIT)對低硒低蛋白大鼠心肌損傷在生化水平上的特點.方法 48隻4週齡Wistar雄性大鼠,2×2析因設計,按體質量隨機分為4組:低硒低蛋白加CIT組、低硒低蛋白組、常硒常蛋白加CIT組、常硒常蛋白組,每組12隻.分彆採用低硒低蛋白和常硒常蛋白飼料餵養大鼠至第12週後,加毒素組大鼠飼料中加入8mg·kg-1·d-1 CIT餵養至第20週,再加量至10 mg·kg-1·d-1 CIT繼續餵養至22週,股動脈採血及取心髒,檢測血清肌鈣蛋白Ⅰ(Tn-Ⅰ)、白蛋白水平,肌痠激酶(CK)、穀胱甘肽過氧化物酶( GSH-Px)以及心肌超氧化物歧化酶(SOD)活性,總抗氧化能力(T-AOC).結果 “硒+蛋白”與CIT對大鼠終來體質量、白蛋白和Tn-Ⅰ存在交互作用(F值分彆為8.186、6.160、19.183,P均＜0.05),對12週大鼠體質量,22週血清GSH-Px、CK水平以及心肌SOD、T-AOC活性的影響不存在交互作用(F值分彆為1.633、1.987、0.075、0.474、1.145,P均＞ 0.05).在低硒低蛋白揹景下,加CIT組血清白蛋白和Tn-Ⅰ水平[(42.88±1.19)g/L,(668.6±55.8) ng/L]均低于無CIT組[(47.59±1.05)g/L,(989.3±49.2)ng/L,P均＜0.05].“硒+蛋白”對12週大鼠體質量、22週血清GSH-Px活性以及心肌SOD、T-AOC有影響(F值分彆為96.860、58.086、4.475、25.485,P均＜0.05).低硒低蛋白兩組12週大鼠體質量[(186.33±7.89)、(197.83±7.89)g]均低于常硒常蛋白兩組[(274.08±7.89)、(265.42±7.89)g,P均＜0.05]；低硒低蛋白兩組[(317.5±102.6)、(296.9±90.5)U/L]血清GSH-Px活性均低于常硒常蛋白兩組[(926.1±110.9)、(1181.7±85.9) U/L,P均＜0.05]；低硒低蛋白兩組心肌SOD活性[ (65.22±5.91)×106、(62.68±5.61)× 106 U/kg]均低于常硒常蛋白兩組[(74.07±7.24)×106、(80.07±5.91)×106 U/kg,P均＜0.05]；低硒低蛋白兩組心肌T-AOC活性[(1.138±0.086)×106、(0.806±0.081)× 106U/kg]均低于常硒常蛋白兩組[(1.688±0.105)×106、(1.163±0.086)×106 U/kg,P均＜0.05].結論 低硒低蛋白模型複製成功,CIT對低硒低蛋白大鼠心肌損傷在生化水平未髮現有規律性效應,有待進一步研究確定.
목적 관찰황록청매소(CIT)대저서저단백대서심기손상재생화수평상적특점.방법 48지4주령Wistar웅성대서,2×2석인설계,안체질량수궤분위4조:저서저단백가CIT조、저서저단백조、상서상단백가CIT조、상서상단백조,매조12지.분별채용저서저단백화상서상단백사료위양대서지제12주후,가독소조대서사료중가입8mg·kg-1·d-1 CIT위양지제20주,재가량지10 mg·kg-1·d-1 CIT계속위양지22주,고동맥채혈급취심장,검측혈청기개단백Ⅰ(Tn-Ⅰ)、백단백수평,기산격매(CK)、곡광감태과양화물매( GSH-Px)이급심기초양화물기화매(SOD)활성,총항양화능력(T-AOC).결과 “서+단백”여CIT대대서종래체질량、백단백화Tn-Ⅰ존재교호작용(F치분별위8.186、6.160、19.183,P균＜0.05),대12주대서체질량,22주혈청GSH-Px、CK수평이급심기SOD、T-AOC활성적영향불존재교호작용(F치분별위1.633、1.987、0.075、0.474、1.145,P균＞ 0.05).재저서저단백배경하,가CIT조혈청백단백화Tn-Ⅰ수평[(42.88±1.19)g/L,(668.6±55.8) ng/L]균저우무CIT조[(47.59±1.05)g/L,(989.3±49.2)ng/L,P균＜0.05].“서+단백”대12주대서체질량、22주혈청GSH-Px활성이급심기SOD、T-AOC유영향(F치분별위96.860、58.086、4.475、25.485,P균＜0.05).저서저단백량조12주대서체질량[(186.33±7.89)、(197.83±7.89)g]균저우상서상단백량조[(274.08±7.89)、(265.42±7.89)g,P균＜0.05]；저서저단백량조[(317.5±102.6)、(296.9±90.5)U/L]혈청GSH-Px활성균저우상서상단백량조[(926.1±110.9)、(1181.7±85.9) U/L,P균＜0.05]；저서저단백량조심기SOD활성[ (65.22±5.91)×106、(62.68±5.61)× 106 U/kg]균저우상서상단백량조[(74.07±7.24)×106、(80.07±5.91)×106 U/kg,P균＜0.05]；저서저단백량조심기T-AOC활성[(1.138±0.086)×106、(0.806±0.081)× 106U/kg]균저우상서상단백량조[(1.688±0.105)×106、(1.163±0.086)×106 U/kg,P균＜0.05].결론 저서저단백모형복제성공,CIT대저서저단백대서심기손상재생화수평미발현유규률성효응,유대진일보연구학정.
Objective To clarify the causative effect of citreoviridin toxins(CIT) as well as nutritional deficiency of selenium and protein on rat myocardial injury at biochemical level.Methods According to 2 × 2 factorial design,48 healthy male Wistar rats aged 4-week were randomly divided into four groups:exposed to CIT along with nutritional deficiency of selenium and protein,nutritional deficiency of selenium and protein,exposed to CIT and control groups.After the rats in each group began to be fed with selenium and protein deficiency and(or) adequate fodder for 3 months,8 mg/kg body weight of CIT was fed daily to the rats in the two CIT toxin groups for two months.After that the CIT dose was raised up to 10 mg/kg body weight each day within the final 2 weeks.At the experimental endpoint,all the rats were sacrificed by femoral artery bleeding after ether anesthesia,and serum and heart specimens were collected for biochemical analysis by detecting serum Tn-Ⅰ and albumin,serum activities of CK and GSH-Px,myocardial SOD and T-AOC.Results The interactions between "Se & protein" and CIT in rat final body weight,serum albumin,and Tn-Ⅰ was observed(F=8.186,6.160,19.183,all P＜ 0.05),whereas interactions in rat body weight of 12 weeks,serum GSH-Px,CK as well as myocardial SOD,T-AOC activity were not found (F=1.633,1.987,0.075,0.474,1.145,all P ＞ 0.05).Under the nutritional deficiency of selenium and protein,serum albumin and Tn-Ⅰ level in the groups with CIT toxin[ (42.88 ± 1.19) g/L,(668.6 ± 55.8) ng/L,respectively]were lower than that of the group without CIT toxin[ (47.59 ± 1.05)g/L,(989.3 ± 49.2)ng/L,respectively,all P ＜0.05].The main effects of selenium and protein on rat body weight of 12 weeks,serum GSH-Px,myocardial SOD and T-AOC were statistically significant between different groups (F =96.860,58.086,4.475,25.485,all P ＜ 0.05).Rat body weights of 12 weeks in the two groups of nutritional deficiency of selenium and protein[ (186.33 ± 7.89),(197.83 ± 7.89)g] were all lower than others[ (274.08 ± 7.89),(265.42 ± 7.89)g,all P ＜ 0.05]; serum GSH-Pxs in the two groups of nutritional deficiency of selenium and protein[ (317.5 ± 102.6),(296.9 ± 90.5)U/L] were all lower than others[ (926.1 ± 110.9),( 1181.7 ± 85.9)U/L,all P ＜ 0.05] ; myocardial SODs in the two groups of nutritional deficiency of selenium and protein [ (65.22 ± 5.91 ) × 106, (62.68 ± 5.61 ) × 106 U/kg] were all lower than others [(74.07 ± 7.24) × 106, (80.07 ± 5.91) × 106 U/kg,all P＜ 0.05]; myocardial T-AOCs in the two groups of nutritional deficiency of selenium and protein[ (1.138 ± 0.086) × 106,(0.806 ± 0.081 ) × 106 U/kg] were all lower than others[(1.688 ± 0.105) × 106,(1.163 ± 0.086) × 106 U/kg,all P ＜ 0.05].Conclusions Animal model with selenium and protein deficiency is successfully established.However,the results of biochemical index tested in the experimental rats show no regularity effect,which needs to be checked again in the future study.
