中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2015年
1期
30-33
,共4页
AKR1C3%子痫前期%动物模型%格列苯脲%肾损伤
AKR1C3%子癇前期%動物模型%格列苯脲%腎損傷
AKR1C3%자간전기%동물모형%격렬분뇨%신손상
AKR1C3%Preeclampsia%Animal model%Glyburide%Kidney damage
目的 探讨AKR1C3对子痫前期大鼠肾脏损伤的影响及其可能的作用机制.方法 通过腹腔注射亚硝基左旋精氨酸甲酯(L-NAME)建立大鼠子痫前期的模型,治疗组同时采用灌胃的方法口服格列苯脲.40只Wistar雌鼠随机分为子痫前期组(孕鼠+L-NAME)、治疗组(孕鼠+L-NAME+格列苯脲)、未孕组(L-NAME)、对照组(孕鼠+生理盐水),每组10只.通过测血压、24 h尿蛋白和透射电镜观察肾脏结构确认子痫前期大鼠造模成功,采用RT-PCR、免疫印迹检测大鼠肾脏AKR1C3蛋白及mRNA含量,Elisa方法检测超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)的浓度.结果 造模前各组大鼠的血压值差异无统计学意义;造模后子痫前期组血压明显高于对照组与治疗组[(143.83±9.62)比(120.83±4.31)及(129.43±14.41) mmHg,均P＜0.05].造模前各组大鼠的24 h尿蛋白含量无差异;造模后子痫前期组的24h尿蛋白含量明显高于对照组与治疗组.子痫前期组大鼠肾脏中AKR1 C3蛋白及mRNA表达水平明显低于对照组[(0.48±0.09)比(0.98 ±0.27)、(0.05 ±0.02)比(0.87±0.45),均P＜0.05].与子痫前期组相比,治疗组AKR1 C3蛋白及mRNA表达水平升高[(0.48±0.09)比(1.05±0.20)、(0.05±0.02)比(0.22 ±0.06),均P＜0.05].与对照组相比子痫前期组SOD、CAT、GSH-Px的浓度明显降低,MDA的浓度升高;与子痫前期组相比,治疗组SOD、CAT、GSH-Px的浓度升高,MDA的浓度降低.结论 AKR1C3在子痫前期大鼠肾脏中表达降低,其作用途径可能与氧化应激有关.格列苯脲对子痫前期的治疗有一定的疗效.
目的 探討AKR1C3對子癇前期大鼠腎髒損傷的影響及其可能的作用機製.方法 通過腹腔註射亞硝基左鏇精氨痠甲酯(L-NAME)建立大鼠子癇前期的模型,治療組同時採用灌胃的方法口服格列苯脲.40隻Wistar雌鼠隨機分為子癇前期組(孕鼠+L-NAME)、治療組(孕鼠+L-NAME+格列苯脲)、未孕組(L-NAME)、對照組(孕鼠+生理鹽水),每組10隻.通過測血壓、24 h尿蛋白和透射電鏡觀察腎髒結構確認子癇前期大鼠造模成功,採用RT-PCR、免疫印跡檢測大鼠腎髒AKR1C3蛋白及mRNA含量,Elisa方法檢測超氧化物歧化酶(SOD)、過氧化氫酶(CAT)、穀胱甘肽過氧化物酶(GSH-Px)、丙二醛(MDA)的濃度.結果 造模前各組大鼠的血壓值差異無統計學意義;造模後子癇前期組血壓明顯高于對照組與治療組[(143.83±9.62)比(120.83±4.31)及(129.43±14.41) mmHg,均P＜0.05].造模前各組大鼠的24 h尿蛋白含量無差異;造模後子癇前期組的24h尿蛋白含量明顯高于對照組與治療組.子癇前期組大鼠腎髒中AKR1 C3蛋白及mRNA錶達水平明顯低于對照組[(0.48±0.09)比(0.98 ±0.27)、(0.05 ±0.02)比(0.87±0.45),均P＜0.05].與子癇前期組相比,治療組AKR1 C3蛋白及mRNA錶達水平升高[(0.48±0.09)比(1.05±0.20)、(0.05±0.02)比(0.22 ±0.06),均P＜0.05].與對照組相比子癇前期組SOD、CAT、GSH-Px的濃度明顯降低,MDA的濃度升高;與子癇前期組相比,治療組SOD、CAT、GSH-Px的濃度升高,MDA的濃度降低.結論 AKR1C3在子癇前期大鼠腎髒中錶達降低,其作用途徑可能與氧化應激有關.格列苯脲對子癇前期的治療有一定的療效.
목적 탐토AKR1C3대자간전기대서신장손상적영향급기가능적작용궤제.방법 통과복강주사아초기좌선정안산갑지(L-NAME)건립대서자간전기적모형,치료조동시채용관위적방법구복격렬분뇨.40지Wistar자서수궤분위자간전기조(잉서+L-NAME)、치료조(잉서+L-NAME+격렬분뇨)、미잉조(L-NAME)、대조조(잉서+생리염수),매조10지.통과측혈압、24 h뇨단백화투사전경관찰신장결구학인자간전기대서조모성공,채용RT-PCR、면역인적검측대서신장AKR1C3단백급mRNA함량,Elisa방법검측초양화물기화매(SOD)、과양화경매(CAT)、곡광감태과양화물매(GSH-Px)、병이철(MDA)적농도.결과 조모전각조대서적혈압치차이무통계학의의;조모후자간전기조혈압명현고우대조조여치료조[(143.83±9.62)비(120.83±4.31)급(129.43±14.41) mmHg,균P＜0.05].조모전각조대서적24 h뇨단백함량무차이;조모후자간전기조적24h뇨단백함량명현고우대조조여치료조.자간전기조대서신장중AKR1 C3단백급mRNA표체수평명현저우대조조[(0.48±0.09)비(0.98 ±0.27)、(0.05 ±0.02)비(0.87±0.45),균P＜0.05].여자간전기조상비,치료조AKR1 C3단백급mRNA표체수평승고[(0.48±0.09)비(1.05±0.20)、(0.05±0.02)비(0.22 ±0.06),균P＜0.05].여대조조상비자간전기조SOD、CAT、GSH-Px적농도명현강저,MDA적농도승고;여자간전기조상비,치료조SOD、CAT、GSH-Px적농도승고,MDA적농도강저.결론 AKR1C3재자간전기대서신장중표체강저,기작용도경가능여양화응격유관.격렬분뇨대자간전기적치료유일정적료효.
Objective To explore the effects of AKR1 C3 on kidney damage of preeclamptic rats and elucidate the possible therapeutic mechanism of glyburide.Methods The rat model of preeclampsia was established by an intraperitoneal injection of Nw-nitro-L-arginine methyl ester hydrochloride (L-NAME).A total of 40 Wistar rats were randomly divided into 4 groups of preeclampsia (pregnant rats and L-NAME),treatment (pregnant rats,L-NAME and glyburide),non-pregnancy (L-NAME) and control (pregnant rats and NS) (n =10 each).The rats in treatment group received an intragastric dose of glyburide.Successful modeling was confirmed by measuring blood pressure and 24 h urine protein content and observing the structure of kidney under transmission electron microscopy (TEM).The methods of reverse transcriptionpolymerase chain reaction (RT-PCR) and Western blot were employed to detect the expression levels of AKR1C3,superoxide dismutase (SOD),catalase (CAT),glutathione peroxidase (GSH-Px) and malondialdehyde (MDA).Results The blood pressures of all rats had no significant difference prior to modeling.After modeling,the blood pressure of preeclampsia group was significantly higher than those of control and treatment groups [(143.83 ±9.62),(120.83 ±4.31),(129.43 ± 14.4) mmHg,both P ＜ 0.05].The 24 h urine protein content of all rats had no significant difference prior to modeling.After modeling,the 24 h urine protein content of preeclampsia group was higher than those of control and treatment groups.The TEM observation of kidney slices verified the success of modeling.In preeclampsia group,the expression levels of AKR1 C3 in protein and mRNA were significantly lower than control group [(0.48 ± 0.09) vs (0.98 ±0.27),(0.05 ± 0.02) vs (0.87 ± 0.45),both P ＜0.05].Compared with preeclampsia group,the expression levels of AKR1C3 in protein and mRNA significantly increased in treatment group [(0.48 ± 0.09) vs (1.05 ± 0.20),(0.05 ± 0.02) vs (0.22 ± 0.06),both P ＜ 0.05].As compared with control group,the levels of SOD,CAT and GSH-Px were significantly lower while MDA was higher.Compared with preeclampsia group,the levels of SOD,CAT and GSH-Px in treatment group were significantly higher while MDA was lower.Conclusion The expression level of AKR1 C3 decreases in kidney of preeelamptic rats and the mechanism is related with oxidative stress.Glyburide increases the expression of AKR1 C3 and have therapeutic effect for preeclampsia.
