临床儿科杂志
臨床兒科雜誌
림상인과잡지
2013年
8期
762-767
,共6页
刘君%黄倩%赵德安%韩子明
劉君%黃倩%趙德安%韓子明
류군%황천%조덕안%한자명
肾小管间质纤维化%单侧输尿管梗阻%硫化氢%大鼠
腎小管間質纖維化%單側輸尿管梗阻%硫化氫%大鼠
신소관간질섬유화%단측수뇨관경조%류화경%대서
tubulointerstitial ifbrosis%uniliteral ureteral obstruction%hydrogen sulifde%rat
目的观察单侧输尿管梗阻（UUO）诱导肾小管间质纤维化（TIF）大鼠模型α-平滑肌肌动蛋白（α-SMA）、Ⅲ型胶原（Col-Ⅲ）表达的变化，以及外源性补充硫化氢（H2S）供体硫氢化钠（NaHS）的干预效果。方法96只SD大鼠随机分为假手术组、模型组、NaHS高剂量组、低剂量组。UUO诱导建立SD大鼠TIF动物模型。高、低剂量组分别于术后立即腹腔注射NaHS 1.4μmol/kg和7.0μmol/kg，2次/d。假手术组和模型组腹腔注射等量生理盐水。各组分别于UUO术后第7、14及21天随机处死8只，采用去蛋白法测定血浆H2S含量；HE及Masson染色观察肾脏病理学变化并评估TIF指数；免疫组化方法检测肾组织α-SMA、Col-Ⅲ表达。结果模型组大鼠梗阻侧肾脏受损，TIF指数升高，经NaHS干预后高、低剂量组的TIF指数均下降，除高、低剂量组的差异无统计学意义外，其余各组间的差异均有统计学意义（P<0.01）；外源性补充NaHS可下调肾组织α-SMA、Col-Ⅲ表达，差异有统计学意义（P<0.05)，但低、高剂量组差异无统计学意义（P>0.05）。结论 UUO诱导TIF与内源性H2S水平降低相关，外源性补充NaHS部分通过下调肾组织α-SMA、Col-Ⅲ表达，延缓TIF进展；但外源性补充H2S在抗TIF中不存在剂量依赖性。
目的觀察單側輸尿管梗阻（UUO）誘導腎小管間質纖維化（TIF）大鼠模型α-平滑肌肌動蛋白（α-SMA）、Ⅲ型膠原（Col-Ⅲ）錶達的變化，以及外源性補充硫化氫（H2S）供體硫氫化鈉（NaHS）的榦預效果。方法96隻SD大鼠隨機分為假手術組、模型組、NaHS高劑量組、低劑量組。UUO誘導建立SD大鼠TIF動物模型。高、低劑量組分彆于術後立即腹腔註射NaHS 1.4μmol/kg和7.0μmol/kg，2次/d。假手術組和模型組腹腔註射等量生理鹽水。各組分彆于UUO術後第7、14及21天隨機處死8隻，採用去蛋白法測定血漿H2S含量；HE及Masson染色觀察腎髒病理學變化併評估TIF指數；免疫組化方法檢測腎組織α-SMA、Col-Ⅲ錶達。結果模型組大鼠梗阻側腎髒受損，TIF指數升高，經NaHS榦預後高、低劑量組的TIF指數均下降，除高、低劑量組的差異無統計學意義外，其餘各組間的差異均有統計學意義（P<0.01）；外源性補充NaHS可下調腎組織α-SMA、Col-Ⅲ錶達，差異有統計學意義（P<0.05)，但低、高劑量組差異無統計學意義（P>0.05）。結論 UUO誘導TIF與內源性H2S水平降低相關，外源性補充NaHS部分通過下調腎組織α-SMA、Col-Ⅲ錶達，延緩TIF進展；但外源性補充H2S在抗TIF中不存在劑量依賴性。
목적관찰단측수뇨관경조（UUO）유도신소관간질섬유화（TIF）대서모형α-평활기기동단백（α-SMA）、Ⅲ형효원（Col-Ⅲ）표체적변화，이급외원성보충류화경（H2S）공체류경화납（NaHS）적간예효과。방법96지SD대서수궤분위가수술조、모형조、NaHS고제량조、저제량조。UUO유도건립SD대서TIF동물모형。고、저제량조분별우술후립즉복강주사NaHS 1.4μmol/kg화7.0μmol/kg，2차/d。가수술조화모형조복강주사등량생리염수。각조분별우UUO술후제7、14급21천수궤처사8지，채용거단백법측정혈장H2S함량；HE급Masson염색관찰신장병이학변화병평고TIF지수；면역조화방법검측신조직α-SMA、Col-Ⅲ표체。결과모형조대서경조측신장수손，TIF지수승고，경NaHS간예후고、저제량조적TIF지수균하강，제고、저제량조적차이무통계학의의외，기여각조간적차이균유통계학의의（P<0.01）；외원성보충NaHS가하조신조직α-SMA、Col-Ⅲ표체，차이유통계학의의（P<0.05)，단저、고제량조차이무통계학의의（P>0.05）。결론 UUO유도TIF여내원성H2S수평강저상관，외원성보충NaHS부분통과하조신조직α-SMA、Col-Ⅲ표체，연완TIF진전；단외원성보충H2S재항TIF중불존재제량의뢰성。
Objectives To observe the expressions ofα-smooth muscle actin (a-SMA) and type III collagen (Col-III) of tubuloin-terstitial ifbrosis(TIF) induced by unilateral ureteral obstruction (UUO) in rat and the intervention effect of supplemental hydrogen sul-ifde (H2S). Methods Ninety-six male Sprague-Dawley rats were randomly divided into 4 groups, sham-operated group, UUO model group, NaHS low-dose group and high-dose group. TIF rat model was established via UUO. After UUO operation, low-dose and high-dose group were intraperitoneally injected twice a day with 1.4μmol/kg and 7.0μmol/kg NaHS, respectively. Sham-operated group and UUO model group were given an equivalent volume of normal saline. Eight rats in each group were killed randomly at 7, 14 and 21 days after UUO operation. The concentration of plasma H2S was detected using deproteinization. Renal tubulointerstitial damage was evaluated with routine Hematoxylin and Eosin staining and Masson staining under microscope. The expressions ofα-SMA, Col-III were measured with immunohistochemistry. Results Compared with sham-operated group, renal tubulointerstitial injury was severer in UUO model group and was alleviated after intervention of NaHS. There was signiifcant difference in tubulointerstitial injury among all groups (P<0.01), but no difference was found between high-dose and low-dose group. Exogenous H2S supplement could down-regu-late the expressions ofα-SMA and Col-III in renal tissues (P<0.05). There was no difference between high-dose and low-dose group in the expressions ofα-SMA and Col-III (P>0.05). Conclusions TIF induced by UUO is associated with decreased level of endogenous H2S. H2S supplementation can ameliorate the development of UUO-associated TIF in part through down-regulating the expressions ofα-SMA and Col-III in renal tissues. However, a dose dependent manner between the two doses of exogenous H2S supplementation was not observed.
