目的 观察姜黄素对饮水型砷中毒大鼠肝脏氧化损伤的干预作用.方法 选取SD大鼠32只,采用随机数字表法按体质量分为4组,每组8只,雌雄各半.正常对照组给予去离子水灌胃135 d;砷中毒对照组按体质量给予10 mg/kg含砷溶液灌胃90d后,再用去离子水灌胃45 d;单纯姜黄素组按体质量给予1 000mg/kg姜黄素溶液灌胃135 d;姜黄素治疗组按体质量给予10 mg/kg含砷溶液灌胃90 d后,再用1 000 mg/kg姜黄素溶液灌胃治疗45 d.采用氢化物发生-电感耦合等离子体发射光谱法(HG-ICP-OES)测定4组大鼠尿砷、肝砷含量;比色法检测血清及肝脏氧化损伤相关指标[铜锌超氧化物歧化酶(Cu/Zn-SOD,简称SOD1)、过氧化氢酶(CAT)活力和丙二醛(MDA)含量];免疫印迹法检测肝脏抗氧化酶SOD1、CAT蛋白表达.结果 与正常对照组大鼠尿砷和肝砷[(0.40±0.14)μg/g Cr,(4.56±1.05)μg/g]含量比较,砷中毒对照组大鼠尿砷[(5.83±0.29)μg/g Cr]和肝砷[(15.76±1.65)μg/g]含量明显升高(P均＜0.05),姜黄素治疗组尿砷[(1.07±0.14)μg/gCr]含量明显升高(P＜0.05);与砷中毒对照组相比,姜黄素治疗组尿砷和肝砷[(5.42±1.76)μg/g]明显下降(P均＜ 0.05).与正常对照组大鼠血清和肝脏SOD1、CAT、MDA含量[(102.46±5.03)、(29.33±8.13)U/ml,(3.11±0.49) μmol/L和(204.05±18.33)、(126.26±13.19)U/mg prot,(1.62±0.42)μmol/g prot]比较,砷中毒对照组和姜黄素治疗组血清和肝脏的SOD1、CAT活力[(60.97±7.94)、(13.56±5.14)U/ml,(133.66±1151)、(74.01±13.30)U/mg prot;(87.39±9.38)、(20.45±6.49)U/ml,(178.27±9.32)、(93.70±20.35)U/mg prot]明显降低,MDA含量[(7.26±0.54)μmol/L,(2.61±0.52)μmol/g prot;(4.34±0.79) μmol/L,(1.92±0.18) μmol/gprot]明显升高(P均＜0.05);与砷中毒对照组相比,姜黄素治疗组血清和肝脏的SOD1、CAT活力升高,MDA含量降低(P均＜ 0.05).与正常对照组大鼠肝脏SOD1、CAT蛋白表达(0.64±0.32、0.72±0.31)相比,单纯姜黄素组SOD1、CAT蛋白表达(1.03±0.23、1.02±0.20)明显升高(P均＜0.05),砷中毒对照组(0.34±0.12、0.39±0.11)明显降低(P均＜0.05);与砷中毒对照组相比,姜黄素治疗组SOD1、CAT蛋白表达(0.58±0.09、0.68±0.29)明显升高(P均＜0.05).大鼠尿砷与肝砷、肝脏MDA含量呈正相关关系[相关系数(r)=0.952、0.732,P均＜0.05],与肝脏SOD1、CAT活力呈负相关关系(r=-0.874、-0.679,P均＜0.05);血清SOD1与肝脏SOD1活力呈正相关关系(r=0.796,P＜0.05);血清CAT活力与肝脏CAT活力呈正相关关系(r=0.484,P＜0.05);血清MDA含量与肝脏MDA含量呈正相关关系(r=0.607,P＜0.05);大鼠肝脏SOD1、CAT活力与SOD1、CAT蛋白表达呈正相关关系(r=0.748、0.424,P均＜0.05).结论 姜黄素可能通过促进砷的排泄及促进肝脏抗氧化酶的蛋白表达,提高砷中毒大鼠肝脏抗氧化酶的活力,有效降低砷所引起的脂质过氧化损害.
目的 觀察薑黃素對飲水型砷中毒大鼠肝髒氧化損傷的榦預作用.方法 選取SD大鼠32隻,採用隨機數字錶法按體質量分為4組,每組8隻,雌雄各半.正常對照組給予去離子水灌胃135 d;砷中毒對照組按體質量給予10 mg/kg含砷溶液灌胃90d後,再用去離子水灌胃45 d;單純薑黃素組按體質量給予1 000mg/kg薑黃素溶液灌胃135 d;薑黃素治療組按體質量給予10 mg/kg含砷溶液灌胃90 d後,再用1 000 mg/kg薑黃素溶液灌胃治療45 d.採用氫化物髮生-電感耦閤等離子體髮射光譜法(HG-ICP-OES)測定4組大鼠尿砷、肝砷含量;比色法檢測血清及肝髒氧化損傷相關指標[銅鋅超氧化物歧化酶(Cu/Zn-SOD,簡稱SOD1)、過氧化氫酶(CAT)活力和丙二醛(MDA)含量];免疫印跡法檢測肝髒抗氧化酶SOD1、CAT蛋白錶達.結果 與正常對照組大鼠尿砷和肝砷[(0.40±0.14)μg/g Cr,(4.56±1.05)μg/g]含量比較,砷中毒對照組大鼠尿砷[(5.83±0.29)μg/g Cr]和肝砷[(15.76±1.65)μg/g]含量明顯升高(P均＜0.05),薑黃素治療組尿砷[(1.07±0.14)μg/gCr]含量明顯升高(P＜0.05);與砷中毒對照組相比,薑黃素治療組尿砷和肝砷[(5.42±1.76)μg/g]明顯下降(P均＜ 0.05).與正常對照組大鼠血清和肝髒SOD1、CAT、MDA含量[(102.46±5.03)、(29.33±8.13)U/ml,(3.11±0.49) μmol/L和(204.05±18.33)、(126.26±13.19)U/mg prot,(1.62±0.42)μmol/g prot]比較,砷中毒對照組和薑黃素治療組血清和肝髒的SOD1、CAT活力[(60.97±7.94)、(13.56±5.14)U/ml,(133.66±1151)、(74.01±13.30)U/mg prot;(87.39±9.38)、(20.45±6.49)U/ml,(178.27±9.32)、(93.70±20.35)U/mg prot]明顯降低,MDA含量[(7.26±0.54)μmol/L,(2.61±0.52)μmol/g prot;(4.34±0.79) μmol/L,(1.92±0.18) μmol/gprot]明顯升高(P均＜0.05);與砷中毒對照組相比,薑黃素治療組血清和肝髒的SOD1、CAT活力升高,MDA含量降低(P均＜ 0.05).與正常對照組大鼠肝髒SOD1、CAT蛋白錶達(0.64±0.32、0.72±0.31)相比,單純薑黃素組SOD1、CAT蛋白錶達(1.03±0.23、1.02±0.20)明顯升高(P均＜0.05),砷中毒對照組(0.34±0.12、0.39±0.11)明顯降低(P均＜0.05);與砷中毒對照組相比,薑黃素治療組SOD1、CAT蛋白錶達(0.58±0.09、0.68±0.29)明顯升高(P均＜0.05).大鼠尿砷與肝砷、肝髒MDA含量呈正相關關繫[相關繫數(r)=0.952、0.732,P均＜0.05],與肝髒SOD1、CAT活力呈負相關關繫(r=-0.874、-0.679,P均＜0.05);血清SOD1與肝髒SOD1活力呈正相關關繫(r=0.796,P＜0.05);血清CAT活力與肝髒CAT活力呈正相關關繫(r=0.484,P＜0.05);血清MDA含量與肝髒MDA含量呈正相關關繫(r=0.607,P＜0.05);大鼠肝髒SOD1、CAT活力與SOD1、CAT蛋白錶達呈正相關關繫(r=0.748、0.424,P均＜0.05).結論 薑黃素可能通過促進砷的排洩及促進肝髒抗氧化酶的蛋白錶達,提高砷中毒大鼠肝髒抗氧化酶的活力,有效降低砷所引起的脂質過氧化損害.
목적 관찰강황소대음수형신중독대서간장양화손상적간예작용.방법 선취SD대서32지,채용수궤수자표법안체질량분위4조,매조8지,자웅각반.정상대조조급여거리자수관위135 d;신중독대조조안체질량급여10 mg/kg함신용액관위90d후,재용거리자수관위45 d;단순강황소조안체질량급여1 000mg/kg강황소용액관위135 d;강황소치료조안체질량급여10 mg/kg함신용액관위90 d후,재용1 000 mg/kg강황소용액관위치료45 d.채용경화물발생-전감우합등리자체발사광보법(HG-ICP-OES)측정4조대서뇨신、간신함량;비색법검측혈청급간장양화손상상관지표[동자초양화물기화매(Cu/Zn-SOD,간칭SOD1)、과양화경매(CAT)활력화병이철(MDA)함량];면역인적법검측간장항양화매SOD1、CAT단백표체.결과 여정상대조조대서뇨신화간신[(0.40±0.14)μg/g Cr,(4.56±1.05)μg/g]함량비교,신중독대조조대서뇨신[(5.83±0.29)μg/g Cr]화간신[(15.76±1.65)μg/g]함량명현승고(P균＜0.05),강황소치료조뇨신[(1.07±0.14)μg/gCr]함량명현승고(P＜0.05);여신중독대조조상비,강황소치료조뇨신화간신[(5.42±1.76)μg/g]명현하강(P균＜ 0.05).여정상대조조대서혈청화간장SOD1、CAT、MDA함량[(102.46±5.03)、(29.33±8.13)U/ml,(3.11±0.49) μmol/L화(204.05±18.33)、(126.26±13.19)U/mg prot,(1.62±0.42)μmol/g prot]비교,신중독대조조화강황소치료조혈청화간장적SOD1、CAT활력[(60.97±7.94)、(13.56±5.14)U/ml,(133.66±1151)、(74.01±13.30)U/mg prot;(87.39±9.38)、(20.45±6.49)U/ml,(178.27±9.32)、(93.70±20.35)U/mg prot]명현강저,MDA함량[(7.26±0.54)μmol/L,(2.61±0.52)μmol/g prot;(4.34±0.79) μmol/L,(1.92±0.18) μmol/gprot]명현승고(P균＜0.05);여신중독대조조상비,강황소치료조혈청화간장적SOD1、CAT활력승고,MDA함량강저(P균＜ 0.05).여정상대조조대서간장SOD1、CAT단백표체(0.64±0.32、0.72±0.31)상비,단순강황소조SOD1、CAT단백표체(1.03±0.23、1.02±0.20)명현승고(P균＜0.05),신중독대조조(0.34±0.12、0.39±0.11)명현강저(P균＜0.05);여신중독대조조상비,강황소치료조SOD1、CAT단백표체(0.58±0.09、0.68±0.29)명현승고(P균＜0.05).대서뇨신여간신、간장MDA함량정정상관관계[상관계수(r)=0.952、0.732,P균＜0.05],여간장SOD1、CAT활력정부상관관계(r=-0.874、-0.679,P균＜0.05);혈청SOD1여간장SOD1활력정정상관관계(r=0.796,P＜0.05);혈청CAT활력여간장CAT활력정정상관관계(r=0.484,P＜0.05);혈청MDA함량여간장MDA함량정정상관관계(r=0.607,P＜0.05);대서간장SOD1、CAT활력여SOD1、CAT단백표체정정상관관계(r=0.748、0.424,P균＜0.05).결론 강황소가능통과촉진신적배설급촉진간장항양화매적단백표체,제고신중독대서간장항양화매적활력,유효강저신소인기적지질과양화손해.
Objective To observe the effects of curcumin on hepatic oxidant stress in water arsenic-exposed rats and to study its mechanism,which can offer references for curcumin used in antioxidant therapy of arsenic poisoning.Methods Thirty-two SD rats were divided into 4 groups according to body weight by random number table,half male and half female.Including control group (lavaged 135 days with deionized water),arsenic poisoning group (lavaged 45 days with deionized water after lavaging 90 days with 10 mg/kg sodium arsenite),pure curcumin group (lavaged 135 days with 1 000 mg/kg curcumin solution) and curcumin treatment group (lavaged 45 days with 1 000 mg/kg curcumin solution after lavaging 90 days with 10 mg/kg sodium arsenite),8 rats in each group.The arsenic contents of urine (urine creatinine corrected) and liver were detected by hydride generation inductively coupled plasma optical emission spectrometer (HG-ICP-OES);the activity of Cu/Zn-superoxide dismutase (SOD1) and catalase (CAT),the contents of malondialdehyde (MDA) in serum and liver homogenate by colorimetric method;the protein expression of liver antioxidant enzyme (SOD 1 and CAT) was assayed by Western blotting.Results The arsenic contents of urine and liver in arsenic poisoning group [(5.83 ± 0.29)μg/g Cr,(15.76 ± 1.65)μg/g] and the arsenic contents of urine in curcumin treatment group [(1.07 ± 0.14)μg/g Cr] were obviously higher than those of control group [(0.40 ± 0.14)μg/g Cr,(4.56 ± 1.05)μg/g,all P ＜ 0.05];compared to arsenic poisoning group,the arsenic contents of urine and liver in curcumin treatment group [(1.07 ± 0.14)μg/g Cr,(5.42 ± 1.76)μg/g] were obviously lower (all P ＜ 0.05).The contents of serum and liver SOD1,CAT and MDA in control group respectively were (102.46 ± 5.03),(29.33 ± 8.13)U/ml,(3.11 ± 0.49)μ mol/L and (204.05 ± 18.33),(126.26 ± 13.19)U/mg prot,(1.62 ± 0.42) μmol/g prot.Compared to the control,the activity of serum and liver SOD1 and CAT in arsenic poisoning group [(60.97 ± 7.94),(13.56 ± 5.14)U/ml and (133.66 ± 11.51),(74.01 ± 13.30)U/mg prot] were lower,the contents of MDA [(7.26 ± 0.54)μmol/L and (2.61 ± 0.52)μmol/g prot] were higher (all P ＜ 0.05).Compared to arsenic poisoning group,the activity of serum and liver SOD1 and CAT in curcumin treatment group [(87.39 ± 9.38),(20.45 ± 6.49) U/ml and (178.27 ± 9.32),(93.70 ± 20.35)U/mg prot] were higher,the contents of MDA [(4.34 ± 0.79)μmol/L and (1.92 ± 0.18)μmol/g prot] were lower (all P ＜ 0.05).The protein expressions of SOD1 and CAT in control group respectively were 0.64 ± 0.32 and 0.72 ± 0.31.Compared to the control group,the protein expressions of SOD1 and CAT in pure curcumin group (1.03 ± 0.23,1.02 ± 0.20) were significantly higher (all P ＜ 0.05) and in arsenic poisoning group (0.34 ± 0.12,0.39 ± 0.11) were lower (all P ＜ 0.05);Compared with the arsenic poisoning group,the protein expressions of SOD1 and CAT in curcumin treatment group (0.58 ± 0.09,0.68 ± 0.29) were significantly higher (all P ＜ 0.05).The arsenic content of urine in rats were positively related with arsenic content of liver and the content of MDA [correlation coefficient (r) =0.952,0.732,all P ＜ 0.05],but negativity related with the activity of SOD1 and CAT in liver (r =-0.874,-0.679,all P ＜ 0.05);the activity of SOD1 and CAT and the content of MDA in serum and liver were positively related (r =0.796,0.484,0.607,all P ＜ 0.05),the activity and protein expression of SOD1 and CAT in liver were positively related (r =0.748,0.424,all P ＜ 0.05).Conclusion The curcumin may improve the activity of hepatic antioxidant enzyme in water arsenic-exposed rats and effectively decrease lipid poroxidation damage caused by arsenic via promoting the excretion of arsenic and the protein expression of hepatic antioxidant enzyme.
