Chinese Journal of Pharmacovigilance ›› 2015, Vol. 12 ›› Issue (10): 582-585.

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Effects of Naringenin on ICAM-1 and NF-κB Activities Following Myocardial Ischemia/Reperfusion Injury

QIAN Xiu-fang, LIU Dan, QIANG Lie-ying   

  1. Department of Pharmacy, Second Hospital of Beijing Armed Police Forces, Beijing 100027, China
  • Received:2015-07-07 Revised:2015-12-07 Online:2015-10-08 Published:2015-12-07

Abstract: 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.

Key words: naringenin, myocardial ischemia/reperfusion injury, ICAM-1, NF-κB

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