摘要
目的建立慢性砷中毒模型,探讨亚砷酸钠对SD大鼠肝脏的损伤作用,同时测定血清相关蛋白含量,为发现早期生物标志物提供依据。方法健康成年SD大鼠112只,雌雄对半,随机分为对照组(A组和E组)、低剂量组(B组和F组)、中剂量组(C组和G组)和高剂量组(D组和H组),共8组,采用自由饮水方式进行染毒,对照组(A、E):0 mg/L,低剂量组(B、F):2 mg/L,中剂量组(C、G):10 mg/L,高剂量组(D、H):50 mg/L,其中A^D组染毒三个月,E^H组染毒6个月,检测大鼠尿砷含量,观察肝脏组织病理学变化,测定血清羧肽酶(CPD)、I型胶原蛋白(COI 1)、大鼠热休克蛋白90α的含量。结果亚砷酸钠染毒3个月和6个月,大鼠肝脏重量基本上呈下降趋势,且在中剂量和高剂量下降较为明显(F=3.246,F=0.989,P<0.05),但肝脏系数变化无统计学意义(F=0.188,F=1.542,P>0.05);随着染毒剂量的增加,肝细胞排列逐渐紊乱,炎性细胞浸润程度增加,肝纤维组织增生,在高剂量组出现肝细胞变性坏死;大鼠血清的羧肽酶(CPD)、热休克蛋白90α(HSP90α)、一型胶原蛋白(COI 1)含量在3个月染毒组差异均无统计学意义(F=1.387,F=0.532,F=1.005,P>0.05),但在6个月染毒组,大鼠羧肽酶(CPD)、一型胶原蛋白(COI 1)差异无统计学意义(F=2.283,F=0.488,P>0.05),热休克蛋白90α(HSP90α)差异具有统计学意义(F=2.086,P<0.05)。结论长期饮水砷暴露可导致肝损伤,热休克蛋白90α在慢性砷中毒中的上调表达提示需要进一步验证热休克蛋白90α是否可以作为早期预警砷中毒的效应指标。
Objective To establish a chronic arsenic poisoning model,explore the liver damage of sodium arsenite on SD rats,and determine the content of serum related proteins in order to provide a basis for the discovery of early biomarkers.Methods A total of 112 healthy adult SD rats,half male and half female were randomly divided into control group(Group A and Group E),low dose group(Group B and Group F),middle dose group(Group C and Group G)and high dose group(Group D and Group H).The rats were divided into 8 groups and exposure to poison by mean of free drinking water:control group(Group A and Group E):0 mg/L,low dose group(Group B and Group F):2 mg/L,middle dose group(Group C and Group G):10 mg/L,high dose group(Group D and Group H):50 mg/L,in which Group A^D was exposed for 3 months,and Group E-H was exposed for 6 months to measure the urinary arsenic content,observe liver histopathological changes,and measure the serum carboxypeptidase(CPD),type I collagen(COI 1)and heat shock protein 90(HSP 90).Results The weight of the rat liver basically showed a downward trend after exposure to sodium arsenite at three and six months,and the decrease was significant at medium and high doses(F=3.246,F=0.989,P<0.05),but the liver coefficient was not statistically significant(F=0.188,F=1.542,P>0.05);With the increase of toxic dose,the arrangement of hepatocytes was gradually disordered,the infiltration degree of inflammatory cells was increased,hepatic fibrosis was proliferated,and hepatocyte degeneration and necrosis occurred in the high-dose group;Carboxypeptidase of rat serum(CPD),heat shock protein 90 alpha(HSP90 alpha),type I collagen(COI)content were observed no statistically significant difference in in the infected group in three months((F=1.387,F=0.532,F=1.005,P>0.05),but in the six months infected group,rats carboxypeptidase(CPD),type I collagen(COI)there was no statistically significant difference((F=2.283,F=0.488,P>0.05).HSP90 showed a statistically significant difference(F=2.086,P<0.05).Conclusion Long-term drinking water arsenic exposure can lead to liver injury.The up-regulation of heat shock protein 90 expression in chronic arsenism suggests that heat shock protein 90 should be used as an early warning indicator of arsenism.
作者
黄佳
张玲
林勤
夏荣香
李小虎
潘凯
马品江
HUANG Jia;ZHANG Ling;LIN Qin;XIA Rong-xiang;LI Xiao-hu;PAN Kai;MA Pin-jiang(The Center for Disease Control and Prevention of Xinjiang Uygur Autonomous Region,Urumqi,830002,China)
出处
《中国地方病防治》
CAS
2019年第4期377-379,共3页
Chinese Journal of Control of Endemic Diseases
基金
国家自然科学基金项目(81560520)