中华小儿外科杂志
中華小兒外科雜誌
중화소인외과잡지
CHINESE JOURNAL OF PEDIATRIC SURGERY
2009年
7期
476-480
,共5页
李凯%曾舒琦%高解春%陈莲
李凱%曾舒琦%高解春%陳蓮
리개%증서기%고해춘%진련
肾母细胞瘤%维生素A缺乏%胚胎发育%维甲类X受体α
腎母細胞瘤%維生素A缺乏%胚胎髮育%維甲類X受體α
신모세포류%유생소A결핍%배태발육%유갑류X수체α
Nephroblastoma%Vitamin A deficiency%Embryonic development%Retinoid X re-ceptor alpha
目的 建立维生素A缺乏的孕鼠模型,观察孕鼠维生素A缺乏对子代鼠胚胎发育和肿瘤发生的作用.方法 取Wismr雌鼠9只,12周龄,体重200～220g.将其分成2组:①维生素A缺乏饮食组6只,受孕前2周起无维生素A饮食直至产后;②正常对照组3只,给予正常饮食.所有雌鼠喂养2周后与健康Wistar公鼠交配成孕鼠.二组孕鼠产后均给予正常饮食,于哺乳期结束后立即处死.分娩后第二天每组分别随机抽取15只新生子代鼠立即处死.其余子代鼠生后给予正常饮食,至生后365 d处死、解剖(如发现中途死亡,即刻解剖).观察二组大鼠产子情况、新生子代鼠血清维生素A浓度、新生子代鼠肾发育形态、子代鼠肿瘤发生率和组织中RXRαmRNA表达.结果 维生素A缺乏饮食组孕鼠产子代鼠51只;正常对照组孕鼠产子代鼠44只.维生素A缺乏饮食组的新生子代鼠血清维生素A浓度为(0.51±0.13)μmol/L,明显低于对照组的新生子代鼠的血清维生素A浓度(0.81±0.15)μmol/L,P=0.000.二组新生子代鼠中均未发现肿瘤组织,但维生素A缺乏饮食组的新生鼠组织中未成熟的肾小球和肾小管较对照组多见.维生素A缺乏组的新生子代鼠双肾中肾源性剩余检出率为60.0%,明显高于对照组(26.7%,P=0.018).维生素A缺乏饮食组子代鼠36只,1只中途死亡,肾母细胞瘤发生率13.9%.对照组的子代鼠无肿瘤发生.维生素A缺乏饮食组子代鼠肾源性剩余检出率30.6%,明显高于对照组子代鼠肾源性剩余检出率(6.9%,P=0.001).子代鼠中肾母细胞瘤组织的RXRαmRNA表达强度为(3.17±0.15),明显低于对照组肾脏组织中RXRαmRNA表达强度(3.58±0.20),P=0.000.结论 大鼠孕期维生素A缺乏会导致子代鼠肾发育差,肾源性剩余增加,肾母细胞瘤发生率增高.维生素A可能通过上调RXRαmRNA的表达来促进肾脏分化和降低肿瘤发生.
目的 建立維生素A缺乏的孕鼠模型,觀察孕鼠維生素A缺乏對子代鼠胚胎髮育和腫瘤髮生的作用.方法 取Wismr雌鼠9隻,12週齡,體重200～220g.將其分成2組:①維生素A缺乏飲食組6隻,受孕前2週起無維生素A飲食直至產後;②正常對照組3隻,給予正常飲食.所有雌鼠餵養2週後與健康Wistar公鼠交配成孕鼠.二組孕鼠產後均給予正常飲食,于哺乳期結束後立即處死.分娩後第二天每組分彆隨機抽取15隻新生子代鼠立即處死.其餘子代鼠生後給予正常飲食,至生後365 d處死、解剖(如髮現中途死亡,即刻解剖).觀察二組大鼠產子情況、新生子代鼠血清維生素A濃度、新生子代鼠腎髮育形態、子代鼠腫瘤髮生率和組織中RXRαmRNA錶達.結果 維生素A缺乏飲食組孕鼠產子代鼠51隻;正常對照組孕鼠產子代鼠44隻.維生素A缺乏飲食組的新生子代鼠血清維生素A濃度為(0.51±0.13)μmol/L,明顯低于對照組的新生子代鼠的血清維生素A濃度(0.81±0.15)μmol/L,P=0.000.二組新生子代鼠中均未髮現腫瘤組織,但維生素A缺乏飲食組的新生鼠組織中未成熟的腎小毬和腎小管較對照組多見.維生素A缺乏組的新生子代鼠雙腎中腎源性剩餘檢齣率為60.0%,明顯高于對照組(26.7%,P=0.018).維生素A缺乏飲食組子代鼠36隻,1隻中途死亡,腎母細胞瘤髮生率13.9%.對照組的子代鼠無腫瘤髮生.維生素A缺乏飲食組子代鼠腎源性剩餘檢齣率30.6%,明顯高于對照組子代鼠腎源性剩餘檢齣率(6.9%,P=0.001).子代鼠中腎母細胞瘤組織的RXRαmRNA錶達彊度為(3.17±0.15),明顯低于對照組腎髒組織中RXRαmRNA錶達彊度(3.58±0.20),P=0.000.結論 大鼠孕期維生素A缺乏會導緻子代鼠腎髮育差,腎源性剩餘增加,腎母細胞瘤髮生率增高.維生素A可能通過上調RXRαmRNA的錶達來促進腎髒分化和降低腫瘤髮生.
목적 건립유생소A결핍적잉서모형,관찰잉서유생소A결핍대자대서배태발육화종류발생적작용.방법 취Wismr자서9지,12주령,체중200～220g.장기분성2조:①유생소A결핍음식조6지,수잉전2주기무유생소A음식직지산후;②정상대조조3지,급여정상음식.소유자서위양2주후여건강Wistar공서교배성잉서.이조잉서산후균급여정상음식,우포유기결속후립즉처사.분면후제이천매조분별수궤추취15지신생자대서립즉처사.기여자대서생후급여정상음식,지생후365 d처사、해부(여발현중도사망,즉각해부).관찰이조대서산자정황、신생자대서혈청유생소A농도、신생자대서신발육형태、자대서종류발생솔화조직중RXRαmRNA표체.결과 유생소A결핍음식조잉서산자대서51지;정상대조조잉서산자대서44지.유생소A결핍음식조적신생자대서혈청유생소A농도위(0.51±0.13)μmol/L,명현저우대조조적신생자대서적혈청유생소A농도(0.81±0.15)μmol/L,P=0.000.이조신생자대서중균미발현종류조직,단유생소A결핍음식조적신생서조직중미성숙적신소구화신소관교대조조다견.유생소A결핍조적신생자대서쌍신중신원성잉여검출솔위60.0%,명현고우대조조(26.7%,P=0.018).유생소A결핍음식조자대서36지,1지중도사망,신모세포류발생솔13.9%.대조조적자대서무종류발생.유생소A결핍음식조자대서신원성잉여검출솔30.6%,명현고우대조조자대서신원성잉여검출솔(6.9%,P=0.001).자대서중신모세포류조직적RXRαmRNA표체강도위(3.17±0.15),명현저우대조조신장조직중RXRαmRNA표체강도(3.58±0.20),P=0.000.결론 대서잉기유생소A결핍회도치자대서신발육차,신원성잉여증가,신모세포류발생솔증고.유생소A가능통과상조RXRαmRNA적표체래촉진신장분화화강저종류발생.
Objective To establish the pregnant rat model of vitamin A deficiency and evaluate the effect of vitamin A deficiency on renal embryonic development and tumorigenesis in filial rats. Methods Nine female Wistar rats (aging 12 weeks, weighing 200～220 g) were divided into Vitamin A deficient Group (VAD: 6 rats were given non-vitamin-A diet from two weeks before mating and till delivery) and Normal Diet Group (ND: three rats were given normal diet). All the pregnant rats were given normal diet after delivery and were sacrificed immediately after the breastfeeding period ended. Randomly, fifteen neonate rats from each group were sacrificed on the next day after delivery. The other pups were given normal diet and sacrificed one year later. The level of serum vitamin A, mor-phology of kidney, incidence of tumor formation and RXRα mRNA expression in renal tissue of filial rats were assessed. Results Fifty-one and 44 neonate rats were born in VAD group and ND group re-spectively. The level of serum vitamin A was significantly lower in the VAD group (0.51±0.13 μmol/L) than that in the ND group (0.81±0.15 μmol/L, P=0.000). No tumor was detected in ei-ther group. Significantly, more hypoplastic renal glomeruli and tubules were observed in neonates of the VAD group. The rate of nephrogenic rest (NRs) in the neonate rats in VAD group (60%) was significantly higher than that in the ND group (26.7%, P<0.018). One filial rat in the VAD group died within one year. The incidence of Wilms tumor (WT) was 13.9% in the VAD group and 0% in the ND group. The rate of Nrs in the VAD group(30.6%) was significantly higher than that in the ND group(6.9%, P = 0.001). The expression of RXRα mRNA in tumor tissue of the filial rats in the VAD group (3.17 ± 0.15) was significantly lower than that in the ND group (3.58 ± 0.20, P =0.000). Conclusions Vitamin A deficiency in pregnant rats may result in renal dysplasia, increased NRs and higher incidence of WT in filial rats. Vitamin A can promote renal development and inhibit tumorigenesis, possibly by increased expression of RXRα mRNA.
