Cardioprotective Effect of Quercetin against Ischemia/Reperfusion Injury Is Mediated Through NO System and Mitochondrial K-ATP Channels

(Pages: 184-190)
Ying Liu, M.D., Yi Song, M.D., Siyuan Li, M.D., Li Mo, M.D., *
The Center of Gerontology and Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan, China
The Center of Gerontology and Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan, China
*Corresponding Address: The Center of Gerontology and Geriatrics West China Hospital Sichuan University No. 37 Guoxue Lane Chengdu Sichuan 610041 China Email:molihxyy@sina.com
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Liu Ying, Song Yi, Li Siyuan, Mo Li. Cardioprotective Effect of Quercetin against Ischemia/Reperfusion Injury Is Mediated Through NO System and Mitochondrial K-ATP Channels. Cell J. 2021; 23(2): 184-190.

Abstract

Objective

Quercetin (Que) is a plant-derived polyphenolic compound, that was shown to possess anti-inflammatory activity in myocardial ischemia/reperfusion (I/R) models in vivo; however, detailed mechanisms of its anti-inflammatory effects remain unclear. This study aimed to examine the effects of quercetin postconditioning (QPC) on I/R-induced inflammatory response in a rat model and evaluate the role of the mitochondrial K-ATP (mitoKATP) channels and NO system in this regard.

Materials and Methods

In this experimental study, hearts of male Wistar rats (250 ± 20 g) perused by Langendorff apparatus, were subjected to 30 minutes of global ischemia followed by 55 minutes reperfusion, and Que was added to the perfusion solution immediately at the onset of reperfusion. Creatine kinase (CK) levels in the coronary effluent were measured by spectrophotometry. Interleukin-1 (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) levels were analyzed by an enzyme-linked immunosorbent assay (ELISA) rat specific kit to assess the inflammatory condition of the myocardial tissue.

Results

Our results showed that QPC significantly improved left ventricular developed pressure (LVDP) (P<0.05), and decreased the CK release into the coronary effluent vs. control group (P<0.01). The levels of IL-1β (P<0.01), TNF-α (P<0.01), and IL-6 (P<0.05) were significantly diminished in Que-treated groups when compared to the control group. Inhibiting mitoKATPchannels by 100 μM 5-hydroxydecanoate and blocking NO system by 100 μM L-NAME reversed the cardioprotective effects of Que.

Conclusion

The findings of this study suggested that QPC exerts cardioprotective effects on myocardial I/R injury (MIRI) through inhibition of inflammatory reactions and improvement of contractility potential. Also, mitoKATP channels and NO system might be involved in this anti-inflammatory effect.