肾衰2号方对慢性肾衰大鼠肾皮质环氧化酶2及环氧化酶1 mRNA表达的影响(英文)

Effects of No.2 Renal Failure Recipe on expressions of cyclooxygenase-2 and-1 mRNAs in rats with chronic renal failure

目的:观察肾衰2号方对慢性肾衰(chronic renal failure,CRF)大鼠肾皮质环氧化酶2(cyclooxygenase-2,COX-2)及环氧化酶1(cyclooxygenase-1,COX-1)mRNA 表达的影响。方法:采用左肾动脉的2/3分支结扎,右肾摘除(ablation/infarction,A/I)法制作大鼠 CRF 模型。造模成功后,将造模大鼠随机分为模型组、西乐葆(塞来昔布)组、肾衰2号方组。选用10只正常大鼠作为正常对照组。治疗2个月后,苏木精和伊红染色观察大鼠肾组织形态学改变,检测治疗前后大鼠血清肌酐(serumcreatinine,SCr)、尿素氮(blood urea nitrogen,BUN)水平,并用逆转录实时聚合酶链反应检测肾组织中COX-2和 COX-1 mRNA 的表达。结果:肾衰2号方能明显降低 CRF 大鼠 SCr 和 BUN 水平,改善肾功能及肾组织形态,并能明显降低 CRF 大鼠肾皮质 COX-2 mRNA 表达量,但对 COX-1 mRNA 表达无明显影响。结论:肾衰2号方可通过抑制 COX-2 mRNA 的过度表达改善肾功能,减轻肾小球硬化和纤维化。

Objective： To observe the effects of No.2 Renal Failure Recipe （No.2RFR）, a compound traditional Chinese herbal medicine, on expressions of cyclooxygenase-2 （COX-2） and cyclooxygenase-1 （COX-1） mRNAs in rats with chronic renal failure （CRF）. Methods： A rat model of CRF was successfully established by infarction of approximately two-thirds of the left kidney and removal of the right kidney （ablation/infarction, A/I）. Thirty A/I rats were randomly divided into untreated group, celebrex group and No.2RFR group. Another 10 SD rats were selected as normal control group. After 2-month treatment, the pathology of the nephridial tissue was observed with hematoxylin and eosin straining under a light microscope. Renal function including serum creatinine （SCr） and blood urea nitrogen （BUN） was determined by using an automatic biochemical analyzer. Expressions of COX-2 and COX-1 mRNAs in nephridial tissues were detected by reverse transcription-polymerase chain reaction （RT-PCR）. Results： No.2RFR could significantly decrease the levels of SCr and BUN. Renal function and morphology of CRF rats were ameliorated and the expressions of COX-2 mRNA were decreased significantly in the No.2RFR group and the celebrex group, but the expressions of COX-1 mRNA had no differences among the four groups. Conclusion： No.2RFR can improve renal function and reduce glomerular sclerosis and renal fibrosis by inhibiting the over-expression of the COX-2 mRNA.