中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2011年
2期
137-141
,共5页
赵倩%吴益%章子贵%杨三平
趙倩%吳益%章子貴%楊三平
조천%오익%장자귀%양삼평
硒%氟化物中毒%肾%脂质过氧化作用%核因子-κB
硒%氟化物中毒%腎%脂質過氧化作用%覈因子-κB
서%불화물중독%신%지질과양화작용%핵인자-κB
Selenium%Fluoride poisoning%Kidney%Lipid peroxidation%NF-kappa B
目的 观察硒对氟致大鼠肾脏损伤的保护作用,探讨硒的最佳作用剂量及作用靶点.方法 断乳SD雄性大鼠80只,按体质量随机分8组,每组10只.对照组饮用自来水;染氟组饮用50 mg/L的氟化钠溶液;低、中、高硒组分别饮用0.375、0.750、1.500 mg/L的亚硒酸钠溶液;氟+低、中、高硒组分别饮用50 mg/L的氟化钠和0.375、0.750、1.500 mg/L的亚硒酸钠两两组合的溶液.染毒6个月后,测大鼠肾脏组织的氧化水平和核因子κB(NF-κB)的表达量.结果 染氟组大鼠体质量[(695.95±55.89)g]低于对照组[(782.69±56.12)g,P＜0.01],染氟组谷胱甘肽过氧化物酶(GSH-Px)活性[(55.86±5.09)U/mgprot]与对照组[(68.66±4.52)U/mgprot]比较,差异无统计学意义(P＞0.05),但有降低的趋势.染氟组大鼠总抗氧化能力(T-AOC)水平[(7.54±1.35)U/mgprot]低于对照组[(9.03±0.37)U/mgprot,P＜0.05],染氟组丙二醛(MDA)水平[(3.86±0.31)nmol/mgprot]高于对照组[(3.14±0.32)nmol/mgprot,P＜0.05].氟+高硒组GSH-Px活性[(74.99±8.41)U/mgprot]高于染氟组[(55.86±5.09)U/mgprot,P＜0.05],MDA水平[(3.17±0.20)nmol/mgprot]低于染氟组[(3.86±0.31)nmol/mgprot,P＜0.05].染氟组、高硒组和氟+低硒组的NF-κB的表达水平(0.360±0.015,0.367±0.007,0.376±0.006)高于对照组(0.312±0.022,P均＜0.05),氟+高硒组(0.312±0.005)低于染氟组(0.360±0.015,P＜0.05).结论 1.500 mg/L硒是本实验条件下硒对慢性氟中毒致大鼠肾脏损伤的最佳保护作用剂量,NF-κB可能是硒拮抗氟中毒的药物靶点.
目的 觀察硒對氟緻大鼠腎髒損傷的保護作用,探討硒的最佳作用劑量及作用靶點.方法 斷乳SD雄性大鼠80隻,按體質量隨機分8組,每組10隻.對照組飲用自來水;染氟組飲用50 mg/L的氟化鈉溶液;低、中、高硒組分彆飲用0.375、0.750、1.500 mg/L的亞硒痠鈉溶液;氟+低、中、高硒組分彆飲用50 mg/L的氟化鈉和0.375、0.750、1.500 mg/L的亞硒痠鈉兩兩組閤的溶液.染毒6箇月後,測大鼠腎髒組織的氧化水平和覈因子κB(NF-κB)的錶達量.結果 染氟組大鼠體質量[(695.95±55.89)g]低于對照組[(782.69±56.12)g,P＜0.01],染氟組穀胱甘肽過氧化物酶(GSH-Px)活性[(55.86±5.09)U/mgprot]與對照組[(68.66±4.52)U/mgprot]比較,差異無統計學意義(P＞0.05),但有降低的趨勢.染氟組大鼠總抗氧化能力(T-AOC)水平[(7.54±1.35)U/mgprot]低于對照組[(9.03±0.37)U/mgprot,P＜0.05],染氟組丙二醛(MDA)水平[(3.86±0.31)nmol/mgprot]高于對照組[(3.14±0.32)nmol/mgprot,P＜0.05].氟+高硒組GSH-Px活性[(74.99±8.41)U/mgprot]高于染氟組[(55.86±5.09)U/mgprot,P＜0.05],MDA水平[(3.17±0.20)nmol/mgprot]低于染氟組[(3.86±0.31)nmol/mgprot,P＜0.05].染氟組、高硒組和氟+低硒組的NF-κB的錶達水平(0.360±0.015,0.367±0.007,0.376±0.006)高于對照組(0.312±0.022,P均＜0.05),氟+高硒組(0.312±0.005)低于染氟組(0.360±0.015,P＜0.05).結論 1.500 mg/L硒是本實驗條件下硒對慢性氟中毒緻大鼠腎髒損傷的最佳保護作用劑量,NF-κB可能是硒拮抗氟中毒的藥物靶點.
목적 관찰서대불치대서신장손상적보호작용,탐토서적최가작용제량급작용파점.방법 단유SD웅성대서80지,안체질량수궤분8조,매조10지.대조조음용자래수;염불조음용50 mg/L적불화납용액;저、중、고서조분별음용0.375、0.750、1.500 mg/L적아서산납용액;불+저、중、고서조분별음용50 mg/L적불화납화0.375、0.750、1.500 mg/L적아서산납량량조합적용액.염독6개월후,측대서신장조직적양화수평화핵인자κB(NF-κB)적표체량.결과 염불조대서체질량[(695.95±55.89)g]저우대조조[(782.69±56.12)g,P＜0.01],염불조곡광감태과양화물매(GSH-Px)활성[(55.86±5.09)U/mgprot]여대조조[(68.66±4.52)U/mgprot]비교,차이무통계학의의(P＞0.05),단유강저적추세.염불조대서총항양화능력(T-AOC)수평[(7.54±1.35)U/mgprot]저우대조조[(9.03±0.37)U/mgprot,P＜0.05],염불조병이철(MDA)수평[(3.86±0.31)nmol/mgprot]고우대조조[(3.14±0.32)nmol/mgprot,P＜0.05].불+고서조GSH-Px활성[(74.99±8.41)U/mgprot]고우염불조[(55.86±5.09)U/mgprot,P＜0.05],MDA수평[(3.17±0.20)nmol/mgprot]저우염불조[(3.86±0.31)nmol/mgprot,P＜0.05].염불조、고서조화불+저서조적NF-κB적표체수평(0.360±0.015,0.367±0.007,0.376±0.006)고우대조조(0.312±0.022,P균＜0.05),불+고서조(0.312±0.005)저우염불조(0.360±0.015,P＜0.05).결론 1.500 mg/L서시본실험조건하서대만성불중독치대서신장손상적최가보호작용제량,NF-κB가능시서길항불중독적약물파점.
Objective To explore the protective effect of selenium, an antioxidant, on fluoride-induced renal injury in rats and find out the optimal level of selenium against fluoride toxicity and its valid molecular target.Methods All 80 male weanling SD rats were randomly divided into 8 groups by body weight as follows: normal control group(drinking tap water), fluoride exposed group (drinking water containing 50 mg/L of NaF), low, middle,high selenium exposed groups(drinking water containing 0.375, 0.750, 1.500 mg/L of Na2SeO3) and low, middle,high Se-fluoride groups (drinking water containing both 50 mg/L NaF and three doses of Na2SeO3 as abovementioned, respectively). After 6 months, the rats were killed then the oxidation level and nuclear factor κB(NF-κB)expression level in kidney were measured. Results The weight of the fluoride exposed group[(695.95 ± 55.89 )g]was significantly deceased than the controls[(782.69 ± 56.12)g, P ＜ 0.01]. Glutathione peroxidase(GSH-Px)activity of fluoride exposed group[(55.86 ± 5.09)U/mgprot] was not significantly different but decreased. Tatal antioxidant capacity (T-AOC) activity in fluoride exposed group [(7.54 ± 1.35)U/mgprot] significantly decreased than the controls[(9.03 ± 0.37 )U/mgprot, P ＜ 0.05]. In addition, a significant increase of malondialdehyde ( MDA )in fluoride exposed group[(3.86 ± 0.31 )mnol/mgprot, P ＜ 0.05] was observed than the controls[(3.14 ± 0.32)nmol/mgprot, P ＜ 0.05]. GSH-Px activity of high Se-fluoride group[(74.99 ± 8.41 )U/mgprot] was significantly higher than the fluoride exposed group[(55.86 ± 5.09)U/mgprot, P ＜ 0.05] and its MDA level[(3.17 ± 0.20)nmol/mgprot] was lower than the fluoride exposed group[(3.86 ± 0.31 ) nmol/mgprot, P ＜ 0.05]. NF-κB expression levels of fluoride group, high selenium group and low Se-fluoride group(0.360 ± 0.015,0.367 ± 0.007,0.376 ± 0.006,respecyively) were obviously increased compared with the controls(0.312 ± 0.022, P ＜ 0.05); it was significantly lower in high Se-fluoride group(0.312 ± 0.005) than in fluoride exposed group(0.360 ± 0.015, P ＜ 0.05). Conclusions Na2SeO3 of 1.5 mg/L is the optimal dose against chronic fluorosis on kidney injury under this experimental condition.NF-κB is likely to be a target molecule of the selenium as an antagonist on fluorosis.
