医药导报
醫藥導報
의약도보
Herald of Medicine
2015年
11期
1429-1433
,共5页
沈建明%邓妍妍%叶婷婷%勾荣%田少江%王黎萍%李骏峰
瀋建明%鄧妍妍%葉婷婷%勾榮%田少江%王黎萍%李駿峰
침건명%산연연%협정정%구영%전소강%왕려평%리준봉
乌司他丁%损伤,肾,急性%内皮素-1%一氧化氮%一氧化氮合酶,诱生型
烏司他丁%損傷,腎,急性%內皮素-1%一氧化氮%一氧化氮閤酶,誘生型
오사타정%손상,신,급성%내피소-1%일양화담%일양화담합매,유생형
Ulinastatin%Injury,kidney,acute%Endothelin-1%Nitric oxide%Nitric oxide synthase,induced
目的：观察乌司他丁对中毒性急性肾损伤(AKI)大鼠肾脏内皮素1(ET￣1)和一氧化氮(NO)的影响。方法将24只雄性 SD 大鼠随机分为正常对照组、模型对照组和治疗组。第1~3天,模型对照组和治疗组大鼠皮下注射庆大霉素,制备中毒性 AKI 模型；正常对照组皮下注射0.9％氯化钠注射液。第4天开始,治疗组腹腔注射乌司他丁30000 U.kg－1.d－1,其他两组腹腔注射0.9％氯化钠注射液3 mL.kg－1.d－1,均连续7 d。于第11天检测3组血清肌酐(Cr)、胱抑素 C(Cys C)及尿液肾损伤分子￣1(Kim￣1)、中性粒细胞明胶酶相关脂质运载蛋白(NGAL)浓度,肾组织 ET￣1、ET￣1 mRNA 以及 NO、内皮型 NO 合酶(eNOS)、诱生型 NO 合酶(iNOS)、eNOS mRNA 和 iNOS mRNA 水平。结果与正常对照组比较,模型对照组血清 Cr、Cys C 和尿液 Kim￣1、NGAL 浓度,肾组织 ET￣1、ET￣1 mRNA、NO、iNOS、iNOS mRNA 水平均升高(P<0.01)；与模型对照组比较,治疗组血清 Cr、Cys C,尿液 Kim￣1、NGAL 浓度,肾组织 ET￣1、ET￣1 mRNA、NO、iNOS、iNOS mRNA 水平均降低(均 P<0.01)。3组 eNOS 与 eNOS mRNA 差异无统计学意义。结论乌司他丁通过下调肾组织 ET￣1、iNOS 和 NO 发挥治疗大鼠中毒性 AKI 作用。
目的：觀察烏司他丁對中毒性急性腎損傷(AKI)大鼠腎髒內皮素1(ET￣1)和一氧化氮(NO)的影響。方法將24隻雄性 SD 大鼠隨機分為正常對照組、模型對照組和治療組。第1~3天,模型對照組和治療組大鼠皮下註射慶大黴素,製備中毒性 AKI 模型；正常對照組皮下註射0.9％氯化鈉註射液。第4天開始,治療組腹腔註射烏司他丁30000 U.kg－1.d－1,其他兩組腹腔註射0.9％氯化鈉註射液3 mL.kg－1.d－1,均連續7 d。于第11天檢測3組血清肌酐(Cr)、胱抑素 C(Cys C)及尿液腎損傷分子￣1(Kim￣1)、中性粒細胞明膠酶相關脂質運載蛋白(NGAL)濃度,腎組織 ET￣1、ET￣1 mRNA 以及 NO、內皮型 NO 閤酶(eNOS)、誘生型 NO 閤酶(iNOS)、eNOS mRNA 和 iNOS mRNA 水平。結果與正常對照組比較,模型對照組血清 Cr、Cys C 和尿液 Kim￣1、NGAL 濃度,腎組織 ET￣1、ET￣1 mRNA、NO、iNOS、iNOS mRNA 水平均升高(P<0.01)；與模型對照組比較,治療組血清 Cr、Cys C,尿液 Kim￣1、NGAL 濃度,腎組織 ET￣1、ET￣1 mRNA、NO、iNOS、iNOS mRNA 水平均降低(均 P<0.01)。3組 eNOS 與 eNOS mRNA 差異無統計學意義。結論烏司他丁通過下調腎組織 ET￣1、iNOS 和 NO 髮揮治療大鼠中毒性 AKI 作用。
목적：관찰오사타정대중독성급성신손상(AKI)대서신장내피소1(ET￣1)화일양화담(NO)적영향。방법장24지웅성 SD 대서수궤분위정상대조조、모형대조조화치료조。제1~3천,모형대조조화치료조대서피하주사경대매소,제비중독성 AKI 모형；정상대조조피하주사0.9％록화납주사액。제4천개시,치료조복강주사오사타정30000 U.kg－1.d－1,기타량조복강주사0.9％록화납주사액3 mL.kg－1.d－1,균련속7 d。우제11천검측3조혈청기항(Cr)、광억소 C(Cys C)급뇨액신손상분자￣1(Kim￣1)、중성립세포명효매상관지질운재단백(NGAL)농도,신조직 ET￣1、ET￣1 mRNA 이급 NO、내피형 NO 합매(eNOS)、유생형 NO 합매(iNOS)、eNOS mRNA 화 iNOS mRNA 수평。결과여정상대조조비교,모형대조조혈청 Cr、Cys C 화뇨액 Kim￣1、NGAL 농도,신조직 ET￣1、ET￣1 mRNA、NO、iNOS、iNOS mRNA 수평균승고(P<0.01)；여모형대조조비교,치료조혈청 Cr、Cys C,뇨액 Kim￣1、NGAL 농도,신조직 ET￣1、ET￣1 mRNA、NO、iNOS、iNOS mRNA 수평균강저(균 P<0.01)。3조 eNOS 여 eNOS mRNA 차이무통계학의의。결론오사타정통과하조신조직 ET￣1、iNOS 화 NO 발휘치료대서중독성 AKI 작용。
Objective To investigate the effects of ulinastatin on renal expression of endothelin￣1 and nitric oxide (NO) in rats with toxic acute kidney injury(AKI). Methods Twenty￣four male SD rats were randomly divided into the normal control group,model control group and treatment groups, with 8 rats in each group. Except normal control group, rats were subcutaneously injected with gentamicin (300 mg.kg-1 .d-1 ) for 3 days to establish a model of toxic AKI.Rats in the treatment group were intraperitoneally injected with a 7￣day course of ulinastatin (30 000 U.kg-1 .d-1 ) from the fourth day.While the other two groups were injected with 0.9% sodium chloride injection (3 mL.kg-1 .d-1 ). The serum level of creatinine and cystatin￣C,urinary concentration of kidney injury molecule￣1(Kim￣1) and neutrophil gelatinase￣associated lipocalin (NGAL), level of endothelin￣1 and NO,expression of endothelin￣1 mRNA,endothelial nitric oxide synthase (eNOS),induced nitric oxide synthase (iNOS),eNOS mRNA and iNOS mRNA in homogenate of renal tissues in each group were detected on the eleventh day. Results Compared with the normal control group,serum level of creatinine and Cystatin￣C,urinary concentration of Kim￣1 and NGAL,level of endothelin￣1 and NO,expression of endothelin￣1 mRNA,iNOS and iNOS mRNA in homogenate of renal tissues were higher in model control group (P<0.01, respectively), while which were lower in treatment group than those in model control group ( P < 0. 01, respectively). And no statistical significant difference of eNOS and eNOS mRNA expression in homogenate of renal tissues existed among the three groups. Conclusion Ulinastatin possesses curative role against rat with toxic AKI via down￣regulating renal expression of endothelin￣1,NO and iNOS.
