中国药物警戒
中國藥物警戒
중국약물경계
Chinese Journal of Pharmacovigilance
2015年
10期
582-585
,共4页
柚皮素%心肌缺血再灌注损伤%细胞间黏附分子 -1%核因子 -κB
柚皮素%心肌缺血再灌註損傷%細胞間黏附分子 -1%覈因子 -κB
유피소%심기결혈재관주손상%세포간점부분자 -1%핵인자 -κB
naringenin%myocardial ischemia/reperfusion injury%ICAM-1%NF-κB
目的：探讨柚皮素（NAR）对心肌缺血再灌注（MI/R）损伤大鼠细胞间黏附分子-1（ICAM-1）和核因子-κB （NF-κB）的影响。方法采用结扎左冠脉前降支30 min 再灌注2 h 的方法复制 MI/R 损伤大鼠模型，随机分为5组（n=10）：假手术组，模型组，NAR 高、中、低剂量组（100、50、25 mg·kg-1），于术前1周开始腹腔注射给药，每日1次。再灌注后取心脏，染色法测定心肌梗死面积；免疫组化法测定心肌组织 NF-κB 和 ICAM-1表达情况；取心肌匀浆，髓过氧化物酶（MPO）法测定中性粒细胞浸润情况。结果 NAR 高剂量可缩小心肌梗死面积至32.91%，与模型组（39.78%）比较差异有统计学意义（P <0.05）；NAR 各剂量组心肌 MPO 活力分别降低至330.54、322.74、280.64 U·g-1，与模型组（423.9 U·g-1）比较差异均有统计学意义（P<0.05或 P<0.01）；与模型组（65.22%）比较，NAR 各剂量组心肌组织 ICAM-1阳性表达分别降低到50.12%、44.75%、42.05%（P<0.01）；与模型组（38.41%）比较，NAR 各剂量可使心肌组织 NF-κB 的阳性表达分别降低至32.05%、30.22%、29.16%（P <0.05或 P <0.01）。结论 NAR 预处理通过抑制中性粒细胞浸润，下调 NF-κB 和 ICAM-1的表达，抑制炎症反应，进而实现对 MI/R 所致心肌损伤的保护作用。
目的：探討柚皮素（NAR）對心肌缺血再灌註（MI/R）損傷大鼠細胞間黏附分子-1（ICAM-1）和覈因子-κB （NF-κB）的影響。方法採用結扎左冠脈前降支30 min 再灌註2 h 的方法複製 MI/R 損傷大鼠模型，隨機分為5組（n=10）：假手術組，模型組，NAR 高、中、低劑量組（100、50、25 mg·kg-1），于術前1週開始腹腔註射給藥，每日1次。再灌註後取心髒，染色法測定心肌梗死麵積；免疫組化法測定心肌組織 NF-κB 和 ICAM-1錶達情況；取心肌勻漿，髓過氧化物酶（MPO）法測定中性粒細胞浸潤情況。結果 NAR 高劑量可縮小心肌梗死麵積至32.91%，與模型組（39.78%）比較差異有統計學意義（P <0.05）；NAR 各劑量組心肌 MPO 活力分彆降低至330.54、322.74、280.64 U·g-1，與模型組（423.9 U·g-1）比較差異均有統計學意義（P<0.05或 P<0.01）；與模型組（65.22%）比較，NAR 各劑量組心肌組織 ICAM-1暘性錶達分彆降低到50.12%、44.75%、42.05%（P<0.01）；與模型組（38.41%）比較，NAR 各劑量可使心肌組織 NF-κB 的暘性錶達分彆降低至32.05%、30.22%、29.16%（P <0.05或 P <0.01）。結論 NAR 預處理通過抑製中性粒細胞浸潤，下調 NF-κB 和 ICAM-1的錶達，抑製炎癥反應，進而實現對 MI/R 所緻心肌損傷的保護作用。
목적：탐토유피소（NAR）대심기결혈재관주（MI/R）손상대서세포간점부분자-1（ICAM-1）화핵인자-κB （NF-κB）적영향。방법채용결찰좌관맥전강지30 min 재관주2 h 적방법복제 MI/R 손상대서모형，수궤분위5조（n=10）：가수술조，모형조，NAR 고、중、저제량조（100、50、25 mg·kg-1），우술전1주개시복강주사급약，매일1차。재관주후취심장，염색법측정심기경사면적；면역조화법측정심기조직 NF-κB 화 ICAM-1표체정황；취심기균장，수과양화물매（MPO）법측정중성립세포침윤정황。결과 NAR 고제량가축소심기경사면적지32.91%，여모형조（39.78%）비교차이유통계학의의（P <0.05）；NAR 각제량조심기 MPO 활력분별강저지330.54、322.74、280.64 U·g-1，여모형조（423.9 U·g-1）비교차이균유통계학의의（P<0.05혹 P<0.01）；여모형조（65.22%）비교，NAR 각제량조심기조직 ICAM-1양성표체분별강저도50.12%、44.75%、42.05%（P<0.01）；여모형조（38.41%）비교，NAR 각제량가사심기조직 NF-κB 적양성표체분별강저지32.05%、30.22%、29.16%（P <0.05혹 P <0.01）。결론 NAR 예처리통과억제중성립세포침윤，하조 NF-κB 화 ICAM-1적표체，억제염증반응，진이실현대 MI/R 소치심기손상적보호작용。
Objective To investigate the effects of naringenin (NAR) on ICAM-1 and NF-κB activities in rats following myocardial ischemia/reperfusion (MI/R) injury. Methods Rat model of MI/R injury was established by coronary artery ligation for 30 min followed by 2-hour reperfusion. Then rats were divided randomly into 5 groups (n=10), namely sham, model and NAR groups (100, 50 and 25 mg·kg-1). NAR was administered by intraperitoneal injection once a day for 7 days pre-operation. The size of myocardial infarction was measured by NBT staining after the reperfusion. The myocardial ICAM-1 and NF-κB activities were detected by immunohistochemistry. The MPO activity in heart homogenate was detected by chromatometry to evaluate the neutrophil infiltration. Results NAR (100 mg·kg-1) reduced the size of myocardial infarction to 32.91%, showing a significant difference compared to 39.78%of model group(P<0.05). The MPO activities in NAR groups were 330.54, 322.74 and 280.64 U·g-1, respectively, which were significantly lower than 423.9 U·g-1 of model group (P<0.05 or P<0.01). NAR evidently reduced the ICAM-1 positive rates in heart to 50.12%, 44.75% and 42.05%, respectively, comparing to 65.22% of model group (P<0.01). Similarly, NAR significantly reduced the NF-κB positive rates to 32.05%, 30.22% and 29.16%, respectively, comparing to 38.41% of model group (P<0.05 or P<0.01). Conclusion The myocardial protection of NAR pretreatment in MI/R injury appears to be associated with the inhibition of neutrophil infiltration, expression of ICAM-1 and NF-κB and inflammatory response.
