解放军医学院学报
解放軍醫學院學報
해방군의학원학보
Academic Journal of Chinese Pla Medical School
2013年
10期
1048-1051
,共4页
董娜%武军华%贾培媛%李倩%温新宇%冯泽国%周建平%王玉霞
董娜%武軍華%賈培媛%李倩%溫新宇%馮澤國%週建平%王玉霞
동나%무군화%가배원%리천%온신우%풍택국%주건평%왕옥하
蓖麻毒素%细胞毒性%病理改变
蓖痳毒素%細胞毒性%病理改變
비마독소%세포독성%병리개변
ricin%cytotoxicity%pathological changes
目的:探讨蓖麻毒素对不同细胞的细胞毒性及小鼠各主要组织脏器毒性的基本病理改变。方法应用MTT法检测不同浓度(1 ng/ml,10 ng/ml,100 ng/ml,1μg/ml)蓖麻毒素给药24 h对不同细胞株(Caco-2,MDCK,MDCK-MDR1,HepG2, H1299)的细胞活性的影响;经灌胃方式使小鼠中毒,中毒24 h观察蓖麻毒素对小鼠脏器的基本病理变化,测定相关生化指标,分析蓖麻毒素对小鼠肝肾损伤。结果不同浓度的蓖麻毒素对Caco-2,MDCK,MDCK-MDR1,HepG2和H1299细胞均有一定的毒性,随着毒素浓度的升高,细胞毒性亦呈上升趋势,有明显量效关系,其中MDCK细胞对蓖麻毒素最为敏感。病理学检测显示蓖麻毒素可致小鼠肾小球出血及部分肾血管内皮细胞缺如,肝细胞水肿、近端肠绒毛损伤、轻度坏死性肺炎并有炎性细胞浸润。血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(ALP)、总胆红素(TBIL)、甘油三酯(TG)、肌酐(CREA)均升高,表明小鼠中毒3 h内肝功能和肾功能已出现一定程度的损伤。结论蓖麻毒素通过抑制蛋白质合成而导致细胞坏死。不同细胞对蓖麻毒素具有不同的敏感性,表现为蓖麻毒素中毒早期,动物即可出现严重的肝、肾损伤。
目的:探討蓖痳毒素對不同細胞的細胞毒性及小鼠各主要組織髒器毒性的基本病理改變。方法應用MTT法檢測不同濃度(1 ng/ml,10 ng/ml,100 ng/ml,1μg/ml)蓖痳毒素給藥24 h對不同細胞株(Caco-2,MDCK,MDCK-MDR1,HepG2, H1299)的細胞活性的影響;經灌胃方式使小鼠中毒,中毒24 h觀察蓖痳毒素對小鼠髒器的基本病理變化,測定相關生化指標,分析蓖痳毒素對小鼠肝腎損傷。結果不同濃度的蓖痳毒素對Caco-2,MDCK,MDCK-MDR1,HepG2和H1299細胞均有一定的毒性,隨著毒素濃度的升高,細胞毒性亦呈上升趨勢,有明顯量效關繫,其中MDCK細胞對蓖痳毒素最為敏感。病理學檢測顯示蓖痳毒素可緻小鼠腎小毬齣血及部分腎血管內皮細胞缺如,肝細胞水腫、近耑腸絨毛損傷、輕度壞死性肺炎併有炎性細胞浸潤。血清中穀丙轉氨酶(ALT)、穀草轉氨酶(AST)、堿性燐痠酶(ALP)、總膽紅素(TBIL)、甘油三酯(TG)、肌酐(CREA)均升高,錶明小鼠中毒3 h內肝功能和腎功能已齣現一定程度的損傷。結論蓖痳毒素通過抑製蛋白質閤成而導緻細胞壞死。不同細胞對蓖痳毒素具有不同的敏感性,錶現為蓖痳毒素中毒早期,動物即可齣現嚴重的肝、腎損傷。
목적:탐토비마독소대불동세포적세포독성급소서각주요조직장기독성적기본병리개변。방법응용MTT법검측불동농도(1 ng/ml,10 ng/ml,100 ng/ml,1μg/ml)비마독소급약24 h대불동세포주(Caco-2,MDCK,MDCK-MDR1,HepG2, H1299)적세포활성적영향;경관위방식사소서중독,중독24 h관찰비마독소대소서장기적기본병리변화,측정상관생화지표,분석비마독소대소서간신손상。결과불동농도적비마독소대Caco-2,MDCK,MDCK-MDR1,HepG2화H1299세포균유일정적독성,수착독소농도적승고,세포독성역정상승추세,유명현량효관계,기중MDCK세포대비마독소최위민감。병이학검측현시비마독소가치소서신소구출혈급부분신혈관내피세포결여,간세포수종、근단장융모손상、경도배사성폐염병유염성세포침윤。혈청중곡병전안매(ALT)、곡초전안매(AST)、감성린산매(ALP)、총담홍소(TBIL)、감유삼지(TG)、기항(CREA)균승고,표명소서중독3 h내간공능화신공능이출현일정정도적손상。결론비마독소통과억제단백질합성이도치세포배사。불동세포대비마독소구유불동적민감성,표현위비마독소중독조기,동물즉가출현엄중적간、신손상。
Objective To study the cytotoxicity of ricin to different cells and the pathological changes in major organizations of ricin-intoxicated mice. Methods Twenty-four hours after the mice administered ricin at different concentrations (1 ng/ml, 10 ng/ml, 100 ng/ml, 1μg/ml), its effect on the viability of different cell lines (Caco-2, MDCK, MDCK-MDR1, HepG2, H1299) was assayed by MTT assay, pathological changes in their major organizations were observed, related biochemical indicators were detected, and ricin-induced damage to the liver and kidney of mice was analyzed. Results Different concentrations of ricin showed its toxicity to Caco-2, MDCK, MDCK-MDR1, HepG2, and H1299 cells in a dose-dependent manner, namely its cytotoxicity increased with its concentration. The MDCK cells were most sensitive to ricin. Pathological examination showed that ricin could lead to glomerular bleeding, renovascular endothelial deficit, edema of liver cells, proximal intestinal villus injury, and mild necrotizing pneumonia with inflammatory cell infiltration. The serum levels of ALT, AST, ALP, TBIL, TG and CREA were elevated in the mice, indicating that the liver and renal function of mice were damaged 3 h after they were intoxicated by ricin. Conclusion Ricin can induce the necrosis of cells by inhibiting the synthesis of protein and is manifested as severe liver and kidney injury during its early intoxication. The sensitivity of different cell lines to ricin is different.