目的:观察急性肾损伤大鼠肾组织中尾加压素Ⅱ(UⅡ)及其受体(GPR14)mRNA表达的变化.方法:雄性Wistar大鼠随机分为对照组(10只,灌服生理盐水)和模型组(30只).模型组大鼠给予关木通水煎剂灌胃25 d,于第3、7、15和25 d分别处死5只,停药10 d后2组大鼠全部处死,留取肾脏,用于肾脏病理学和UⅡ、GPR14 mRNA的检测.结果:(1)给药3 d后HE染色可见局部肾小管上皮细胞变性、坏死和崩解,并随给药时间的延长逐渐加重,停药10 d后病变未见减轻反而加重.(2)与对照组比较,模型组UⅡ mRNA在给药15 d后明显升高(P<0.05),25 d后更高(P<0.01),实验结束时最高;GPR14 mRNA在给药7 d后即明显增强(P<0.05),15 d后显著增强(P<0.01),此后随着实验时间的延长逐渐增强.结论:在关木通所致肾损伤中UⅡ及其受体基因表达明显增强,提示UⅡ在急性肾损伤的发生发展中可能有一定的病理作用.%AIM: To observe the mRNA expression of urotensin Ⅱ ( UⅡ ) and its receptor ( G protein - coupled receptor 14, GPR14 ) in nephridial tissues of rats with acute renal damage.METHODS: Male Wistar rats were divided into 2 groups: the rats in control group ( n = 10 ) were administered with normal saline by gavage; the rats in model group ( n = 30 ) were administered with Caulis Aristolochiae manshuriensis ( CAM ) by gavage for 25 d to induce acute renal damage.Every 5 rats in model group were sacrificed on the 3rd, 7th, 15th and 25th days during CAM treatment and all rats in the 2 groups were killed 10 d after withdraw of CAM.The kidneys were collected for pathological observation and the UⅡ and GPR14 mRNA examination.RESULTS: The degeneration, necrosis and disintegration in tubules were observed as major pathological changes in the rat kidneys after 3 d of CAM administration.The pathological changes were aggravated following the duration of in CAM administration, and were remained and even worsen when CAM was withdrawn for 10 d.Compared with control group, the mRNA expression of UⅡ was significantly elevated ( P ＜0.05 ) at the time point of CAM administration for 15 d,even obviously increased (P＜0.01)at the time point of CAM administration for 25 d, and remained at the highest levels to the end of the observation.The mRNA expression of GPR14 was significantly increased ( P ＜0.05 ) at the time point of CAM administration for 7 d, became higher ( P ＜0.01 ) on the 15th day, and gradually increased as the experimental time went on.CONCLUSION: The mRNA levels of UⅡ and its receptor are significantly elevated in CAM -induced renal lesion in rats, suggesting that UⅡ plays a pathological role in the development of acute renal damage.
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