中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2011年
4期
379-383
,共5页
目的 观察黄绿青霉素(CIT)对低硒低蛋白大鼠心肌损伤的特点.方法 40只4周龄Wistar大鼠,雌雄符半,体质量60～80 g,按2×2析因设计随机分为常硒常蛋白无毒素组、常硒常蛋白加毒素组、低硒低蛋白无毒素组和低硒低蛋白加毒素组(将低硒低蛋白合为一种因素考虑),每组10只.分别采用常硒常蛋白和低硒低蛋白饲料喂养大鼠至第10周后,加毒素组大鼠饲料中投予CIT(5 mg·kg-1·d-1)继续喂养至第16周.观察各组大鼠的毛色、摄食、体质量增长情况,计算心脏质量指数,观察心肌病理变化,检测血清硒、白蛋白水平、肌酸激酶(CK)和谷胱甘肽过氧化物酶(GSH-Px)活性以及心肌超氧化物歧化酶(SOD)活性.结果 硒、蛋白和CIT对大鼠体质量、血清硒、白蛋白水平、心脏质量指数、血清CK、GSH-Px活性和心肌SOD活性的影响不存在交互作用(F值分别为0.000、1.210、0.625、0.981、2.785、0.074、0.001,P均>0.05);硒、蛋白对大鼠血清硒、白蛋白水平、心脏质量指数和血清GSH-Px活性的主效应有统计学意义(F值分别为507.698、87.734、4.201、109.389,P均<0.05);CIT对大鼠体质量、血清硒、白蛋白水平、心脏质量指数、血清CK活性的主效应有统计学意义(F值分别为10.929、4.371、26.108、24.844、4.439,P均<0.05).低硒低蛋白两组的血清硒水平[(70.4±40.0)、(87.7 ±59.6)μg/L]低于常硒常蛋A两组[(446.1±74.8)、(502.1±39.2)μg/L,P均<0.05];低硒低蛋白两组的血清白蛋白水平[(34.36±1.28)、(33.38±2.48)g/L]低于常硒常蛋白两组[(40.69±1.30)、(38.71±2.15)g/L,P均<0.05];相同硒和蛋白水平下,加毒素组的心脏质量指数[(4.14±0.36)×10-3、(4.39 ±0.53)×10-3]高于无毒素组[(3.56±0.26)×10-3、(3.80±0.28)×10-3,P均<0.05];低硒低蛋白加毒素组的血清CK活性[(2.54 ±0.56)kU/L]低于低硒低蛋白无毒素组[(3.37±0.67)kU/L,P<0.05].低硒低蛋白两组的血清GSH-Px活性>(408.1±412.6)、(510.5 ±392.0)U/L[低于常硒常蛋白两组[(1667.8±102.2)、(1731.5±144.4)U/L,P均<0.05].电镜结果显示,常硒常蛋白加毒素组大鼠部分心肌细胞闰盘断裂,各带连接断裂,部分区域心肌细胞有溶解现象,有水肿表现;低硒低蛋白无毒素组大鼠心肌细胞膜结构改变不明显,核周围肌丝结构消失,可见大量絮状物质沉积;低硒低蛋白加毒素组大鼠心肌细胞肌节各带结构不很清晰,核旁线粒休嵴轻度疏松,偶见空泡变,大量弥漫性肌质网扩张.结论 CIT是诱导大鼠心肌细胞损伤的主要因素,低硒低蛋白加重病变,但独立致病作用较弱.
目的 觀察黃綠青黴素(CIT)對低硒低蛋白大鼠心肌損傷的特點.方法 40隻4週齡Wistar大鼠,雌雄符半,體質量60～80 g,按2×2析因設計隨機分為常硒常蛋白無毒素組、常硒常蛋白加毒素組、低硒低蛋白無毒素組和低硒低蛋白加毒素組(將低硒低蛋白閤為一種因素攷慮),每組10隻.分彆採用常硒常蛋白和低硒低蛋白飼料餵養大鼠至第10週後,加毒素組大鼠飼料中投予CIT(5 mg·kg-1·d-1)繼續餵養至第16週.觀察各組大鼠的毛色、攝食、體質量增長情況,計算心髒質量指數,觀察心肌病理變化,檢測血清硒、白蛋白水平、肌痠激酶(CK)和穀胱甘肽過氧化物酶(GSH-Px)活性以及心肌超氧化物歧化酶(SOD)活性.結果 硒、蛋白和CIT對大鼠體質量、血清硒、白蛋白水平、心髒質量指數、血清CK、GSH-Px活性和心肌SOD活性的影響不存在交互作用(F值分彆為0.000、1.210、0.625、0.981、2.785、0.074、0.001,P均>0.05);硒、蛋白對大鼠血清硒、白蛋白水平、心髒質量指數和血清GSH-Px活性的主效應有統計學意義(F值分彆為507.698、87.734、4.201、109.389,P均<0.05);CIT對大鼠體質量、血清硒、白蛋白水平、心髒質量指數、血清CK活性的主效應有統計學意義(F值分彆為10.929、4.371、26.108、24.844、4.439,P均<0.05).低硒低蛋白兩組的血清硒水平[(70.4±40.0)、(87.7 ±59.6)μg/L]低于常硒常蛋A兩組[(446.1±74.8)、(502.1±39.2)μg/L,P均<0.05];低硒低蛋白兩組的血清白蛋白水平[(34.36±1.28)、(33.38±2.48)g/L]低于常硒常蛋白兩組[(40.69±1.30)、(38.71±2.15)g/L,P均<0.05];相同硒和蛋白水平下,加毒素組的心髒質量指數[(4.14±0.36)×10-3、(4.39 ±0.53)×10-3]高于無毒素組[(3.56±0.26)×10-3、(3.80±0.28)×10-3,P均<0.05];低硒低蛋白加毒素組的血清CK活性[(2.54 ±0.56)kU/L]低于低硒低蛋白無毒素組[(3.37±0.67)kU/L,P<0.05].低硒低蛋白兩組的血清GSH-Px活性>(408.1±412.6)、(510.5 ±392.0)U/L[低于常硒常蛋白兩組[(1667.8±102.2)、(1731.5±144.4)U/L,P均<0.05].電鏡結果顯示,常硒常蛋白加毒素組大鼠部分心肌細胞閏盤斷裂,各帶連接斷裂,部分區域心肌細胞有溶解現象,有水腫錶現;低硒低蛋白無毒素組大鼠心肌細胞膜結構改變不明顯,覈週圍肌絲結構消失,可見大量絮狀物質沉積;低硒低蛋白加毒素組大鼠心肌細胞肌節各帶結構不很清晰,覈徬線粒休嵴輕度疏鬆,偶見空泡變,大量瀰漫性肌質網擴張.結論 CIT是誘導大鼠心肌細胞損傷的主要因素,低硒低蛋白加重病變,但獨立緻病作用較弱.
목적 관찰황록청매소(CIT)대저서저단백대서심기손상적특점.방법 40지4주령Wistar대서,자웅부반,체질량60～80 g,안2×2석인설계수궤분위상서상단백무독소조、상서상단백가독소조、저서저단백무독소조화저서저단백가독소조(장저서저단백합위일충인소고필),매조10지.분별채용상서상단백화저서저단백사료위양대서지제10주후,가독소조대서사료중투여CIT(5 mg·kg-1·d-1)계속위양지제16주.관찰각조대서적모색、섭식、체질량증장정황,계산심장질량지수,관찰심기병리변화,검측혈청서、백단백수평、기산격매(CK)화곡광감태과양화물매(GSH-Px)활성이급심기초양화물기화매(SOD)활성.결과 서、단백화CIT대대서체질량、혈청서、백단백수평、심장질량지수、혈청CK、GSH-Px활성화심기SOD활성적영향불존재교호작용(F치분별위0.000、1.210、0.625、0.981、2.785、0.074、0.001,P균>0.05);서、단백대대서혈청서、백단백수평、심장질량지수화혈청GSH-Px활성적주효응유통계학의의(F치분별위507.698、87.734、4.201、109.389,P균<0.05);CIT대대서체질량、혈청서、백단백수평、심장질량지수、혈청CK활성적주효응유통계학의의(F치분별위10.929、4.371、26.108、24.844、4.439,P균<0.05).저서저단백량조적혈청서수평[(70.4±40.0)、(87.7 ±59.6)μg/L]저우상서상단A량조[(446.1±74.8)、(502.1±39.2)μg/L,P균<0.05];저서저단백량조적혈청백단백수평[(34.36±1.28)、(33.38±2.48)g/L]저우상서상단백량조[(40.69±1.30)、(38.71±2.15)g/L,P균<0.05];상동서화단백수평하,가독소조적심장질량지수[(4.14±0.36)×10-3、(4.39 ±0.53)×10-3]고우무독소조[(3.56±0.26)×10-3、(3.80±0.28)×10-3,P균<0.05];저서저단백가독소조적혈청CK활성[(2.54 ±0.56)kU/L]저우저서저단백무독소조[(3.37±0.67)kU/L,P<0.05].저서저단백량조적혈청GSH-Px활성>(408.1±412.6)、(510.5 ±392.0)U/L[저우상서상단백량조[(1667.8±102.2)、(1731.5±144.4)U/L,P균<0.05].전경결과현시,상서상단백가독소조대서부분심기세포윤반단렬,각대련접단렬,부분구역심기세포유용해현상,유수종표현;저서저단백무독소조대서심기세포막결구개변불명현,핵주위기사결구소실,가견대량서상물질침적;저서저단백가독소조대서심기세포기절각대결구불흔청석,핵방선립휴척경도소송,우견공포변,대량미만성기질망확장.결론 CIT시유도대서심기세포손상적주요인소,저서저단백가중병변,단독립치병작용교약.
Objective To ohserve the rat myocardial damage induced by citreoviridin(CIT)in the status of combined selenium and protein deficiency.Methods According to 2×2 factorial design,forty 4-week-old healthy Wistar rats were randomly divided into four groups.i.e.combined selenium and protein adequate with no CIT and with some CIT groups(Se+Pro+CIT-.Se+Pro+CiT+),combined selenium and protein deficiency with no CIT and with some CIT groups(Se-Pro-CIT-,Se-Pro-CIT+).The numbers of male and female were fifty-fifty.Theserats were fed with combined selenium and protein adequate and combined selenium and protein deficiency fodder until the 16th week. Cardiac toxicity of CIT was evaluated by general state of health, heart weight index, myocardial pathological change, the levels of selenium and the activities of glutathion peroxidase (GSH-Px) and creatine kinase (CK) in serum, and the activity of superoxide dismutase(SOD) of myocardium. Results The interaction effects of combined selenium and protein deficiency and adequate CIT on body weight, serum levels of selenium and albumin, heart weight index, the activities of CK and GSH-Px in serum and SOD of myocardium were statistically not significant(F= 0.000, 1.210, 0.625, 0.981, 2.785, 0.074, 0.001, all P> 0.05). The main effects of combined selenium and protein on the levels of serum selenium and albumin, heart weight index and the activity of GSH-Px in serum were statistically significant(F = 507.698, 87.734, 4.201, 109.389, all P < 0.05). The main effects of CIT on body weight, the levels of serum selenium and albumin, heart weight index and the activity of CK in serum were statistically significant(F = 10.929, 4.371, 26.108, 24.844, 4.439, all P < 0.05). The mean levels of serum selenium of Se-Pro- groups [(70.4 ± 40.0), (87.7 ± 59.6 )μg/L] were lower than those of Se+Pro+ groups [(446.1 ± 74.8),(502.1 ± 39.2)μg/L, all P < 0.05]. The mean levels of serum albumin of Se-Pro- groups [(34.36 ± 1.28 ), (33.38 ±2.48)g/L] were lower than those of Se+Pro+ groups[(40.69 ± 1.30), (38.71 ± 2.15)g/L, all P < 0.05]. The mean levels of heart weight index of CIT+ groups[(4.14 ± 0.36) × 10-3, (4.39 ± 0.53) x 10-3] were higher than those of CIT-groups[(3.56 ± 0.26) x 10-3, (3.80 ± 0.28) x 10-3, all P < 0.05] respectively at the same levels of selenium and protein. The mean levels of CK in serum of Se-Pro-CIT+ group[(2.54 ± 0.56)kU/L] was lower than that of Se-Pro-CIT- group [(3.37 ± 0.67 )kU/L, P < 0.05]. The mean levels of activity of GSH-Px in serum of Se-Progroups[(408.1 ± 412.6), (510.5 ± 392.0)U/L] were lower than those of Se+Pro+ groups[(1667.8 ± 102.2),(1731.5 ± 144.4)U/L, all P < 0.05]. In Se+Pro+CIT+ group, there was part of intercalary disc of cardiac myocytes fragmented;the conjunctions between myoeytes were broken;in some region, cardiac myocytes became edematous,even dissolved. In Se-Pro-CIT- group, the change of cardiac myocytes membrane structures was not obvious;filament structure was disappeared around nucleus;deposition of mass floccule could be seen. In Se-Pro-CIT+ group,the structure of sarcomeres was not obvious;mitochondrial cristae was loosened;cavities in myocytes could be seen occasionally;there were lots of disseminated sareoplasmic reticulum extending. Conclusions .CIT is the main risk factor in inducing myocardial damage. The deficiency of combined selenium and protein can aggravate the damage,but its independent pathogenic effect is weak.
