CAJ | 학술논문

目的：观察丹酚酸 A、B 及其分子药对配伍对肾纤维化中 CTGF 及 Par-3表达的影响。方法：采用50只雄性 SPF 级SD 大鼠随机分为5组：正常组、造模组、丹酚酸 A 组、丹酚酸 B 组及丹酚酸 A ＋B 组。除正常组外，其余大鼠均造成 UUO模型。各组予相应药物治疗2周，腹主动脉采血检测大鼠 Cr、BUN；免疫荧光观察大鼠肾组织 CTGF、Par-3表达情况。结果：1）肾功能检测：模型组大鼠血清 Cr，BUN 水平显著高于正常组（P ＜0．05）。丹酚酸 A 组大鼠血清 Cr 水平明显低于模型组（P ＜0．05）；丹酚酸 A 组和丹酚酸 B 组大鼠血清 BUN 水平明显低于模型组（P ＜0．05）；各治疗组间比较，血清 Cr 和BUN 水平差异无统计学意义（P ＞0．05）。2）CTGF 免疫荧光检测：和正常组相比，模型组大鼠肾组织肾小管上皮细胞阳性细胞数目明显增多，荧光强度明显增强（＋＋＋）；经丹酚酸 A、B 及组分配伍治疗后，CTGF 荧光强度较模型组明显减弱，其中以丹酚酸 A ＋B 组减弱较为明显（±），丹酚酸 B 组次之（＋）。3）Par-3免疫荧光检测结果：模型组大鼠肾组织肾小管上皮细胞阳性细胞数目比正常组明显减少，荧光强度明显减弱（±）；经丹酚酸 A、B 及组分配伍治疗后，丹酚酸 A、B、A ＋B组 Par-3荧光强度较模型组明显增强，其中以丹酚酸 A ＋B 组增强较为明显（＋＋＋），丹酚酸 B 组次之（＋＋）。结论：经丹酚酸 A、B 及其分子药对配伍治疗后，可一定程度改善大鼠肾功能，但无统计学意义；丹酚酸组分配伍组能显著抑制大鼠肾组织 CTGF 的表达、促进 Par-3的表达，其效果优于丹酚酸 A 和丹酚酸 B 组。该机制可能与其促进 Par-3在 UUO 大鼠肾组织中的表达和减少 CTGF 的表达有关。
목적：관찰단분산 A、B 급기분자약대배오대신섬유화중 CTGF 급 Par-3표체적영향。방법：채용50지웅성 SPF 급SD 대서수궤분위5조：정상조、조모조、단분산 A 조、단분산 B 조급단분산 A ＋B 조。제정상조외，기여대서균조성 UUO모형。각조여상응약물치료2주，복주동맥채혈검측대서 Cr、BUN；면역형광관찰대서신조직 CTGF、Par-3표체정황。결과：1）신공능검측：모형조대서혈청 Cr，BUN 수평현저고우정상조（P ＜0．05）。단분산 A 조대서혈청 Cr 수평명현저우모형조（P ＜0．05）；단분산 A 조화단분산 B 조대서혈청 BUN 수평명현저우모형조（P ＜0．05）；각치료조간비교，혈청 Cr 화BUN 수평차이무통계학의의（P ＞0．05）。2）CTGF 면역형광검측：화정상조상비，모형조대서신조직신소관상피세포양성세포수목명현증다，형광강도명현증강（＋＋＋）；경단분산 A、B 급조분배오치료후，CTGF 형광강도교모형조명현감약，기중이단분산 A ＋B 조감약교위명현（±），단분산 B 조차지（＋）。3）Par-3면역형광검측결과：모형조대서신조직신소관상피세포양성세포수목비정상조명현감소，형광강도명현감약（±）；경단분산 A、B 급조분배오치료후，단분산 A、B、A ＋B조 Par-3형광강도교모형조명현증강，기중이단분산 A ＋B 조증강교위명현（＋＋＋），단분산 B 조차지（＋＋）。결론：경단분산 A、B 급기분자약대배오치료후，가일정정도개선대서신공능，단무통계학의의；단분산조분배오조능현저억제대서신조직 CTGF 적표체、촉진 Par-3적표체，기효과우우단분산 A 화단분산 B 조。해궤제가능여기촉진 Par-3재 UUO 대서신조직중적표체화감소 CTGF 적표체유관。
Objective:To investigate the intervention effect of Salvianolic acid A,B and their component molecules of drug com-patibility on expression of CTGF and Par-3 in the process of renal fibrosis.Methods:A total of 50 male Sprague-Dawley rats were randomly divided into five groups:normal group (n =1 0),the control group (n =1 0),salvianolic acid A group (n =1 0),salvi-anolic acid B group (n =1 0)and salvianolic acid A and B group (n =1 0).All rats were made into unilateral ureteral obstruction (UUO)model except the normal group.After two weeks of treatment,we took blood sample from abdominal aorta and examined Cr and BUN levels;and observed CTGF,Par-3 protein expression in kidney tissue by immunofluorescence.Results:1 )Results of renal function test:model group’s serum Cr level was significantly higher than the normal group (P <0.05);the Sal A group’s ser-um Cr level was obviously lower than the model group (P <0.05);the serum BUN levels in the Sal group A and group B signifi-cantly lower than the model group;among the treatment groups,serum Cr and BUN levels showed no significant difference (P >0.05).2)Results of CTGF immunofluorescence test:the number of rat renal tubular epithelial cells showing positive in model group significantly increased compared to the control group and the fluorescence intensity significantly enhanced (+++);after treatment of Sal A,B,and component compatibility,CTGF fluorescence intensity was reduced compared with the model group ,a-mong which the Sal A +B group decreased significantly (±)and followed by the Sal B group (+).3)Results of Par-3 immuno-fluorescence test:the number of positive cells in rat renal tubular epithelial cells in the model group was significantly decreased than the normal group and the fluorescence intensity was significantly reduced (±);after treatment of Sal A,B and component compatibility,Par-3 the fluorescence intensity in the Sal A,Sal B,Sal A +B group was significantly enhanced compared with the model group ,among which the Sal A +B group enhanced most obviously (+++),and followed by the Sal group B (++). Conclusion:Sal A,B and component compatibility treatment could partly improve rat’s renal function,but showed no significant difference.The Sal A +B group could significantly inhibit the expression of CTGF in renal tissue and promote expression of Par-3, and its effect was better than the Sal A group and Sal B group.It may be related to promoting the expression of Par-3 and reducing the expression of CTGF in UUO kidney tissue of rats.