Abstract
Quercetin is an important dietary flavonoid present in fruits and vegetables and has attracted attention because of its anti-inflammatory and anti-oxidative properties. Inflammation and oxidative stress play important roles in posttraumatic cardiomyocyte apoptosis, which contributes to secondary cardiac dysfunction. This study investigates the protective effect of quercetin on trauma-induced secondary cardiac injury and the mechanisms involved. Widely accepted nonlethal mechanical trauma models were established. In vivo, cardiomyocyte apoptosis and cardiac dysfunction in rats were assessed using TUNEL staining and a biological mechanic experiment system. In vitro, cell viability, tumour necrosis factor-α (TNF-α), reactive oxygen species (ROS) and [Ca2+]i of H9c2 cells were detected using an MTT assay, ELISA, and 2′,7′-dichlorofluorescin diacetate and fluo-4 acetoxymethyl ester assays respectively. Quercetin pretreatment (20 mg/kg i.p.; 0.5 h before trauma) significantly improved posttraumatic cardiomyocyte apoptosis and cardiac dysfunction. Pretreatment with quercetin (20 μM; 24 h before trauma plasma addition) significantly attenuated trauma-induced viability decreases, TNF-α increases, ROS overproduction and [Ca2+]i overload in H9c2 cells. In conclusion, quercetin may reverse posttraumatic cardiac dysfunction by reducing cardiomyocyte apoptosis through the suppression of TNF-α increases, ROS overproduction and Ca2+ overload in cardiomyocytes, representing a potential preventive approach for the treatment of secondary cardiac injury after mechanical trauma.
Highlights
Mechanical trauma (MT), such as that caused during motor vehicle crashes, athletic competition, and war, currently represents a primary economic and medical burden
We have provided clear evidence that TNF-αinitiates cardiomyocyte apoptosis by the overproduction of cytotoxic reactive oxygen/ nitrogen species in cardiomyocytes. These results support the hypothesis that the overproduction of TNF-αand reactive oxygen species (ROS) may be the primary cause of secondary cardiomyocyte apoptosis, which eventually leads to secondary cardiac dysfunction after MT
To determine the most appropriate trauma intensity in the nonlethal MT model, the cardiomyocyte apoptosis states of rats subjected to 0 r, 100 r, 200 r, and 400 r were assessed using TUNEL and DAPI staining 12 h after trauma
Summary
Mechanical trauma (MT), such as that caused during motor vehicle crashes, athletic competition, and war, currently represents a primary economic and medical burden. Our previous study[14] demonstrated that trauma-induced overproduction of TNF-αis the main reason for cardiomyocyte apoptosis, which contributes to posttraumatic cardiac dysfunction. We have provided clear evidence that TNF-αinitiates cardiomyocyte apoptosis by the overproduction of cytotoxic reactive oxygen/ nitrogen species in cardiomyocytes These results support the hypothesis that the overproduction of TNF-αand ROS may be the primary cause of secondary cardiomyocyte apoptosis, which eventually leads to secondary cardiac dysfunction after MT. Quercetin is a natural flavonoid compound that is widely distributed in fruits and vegetables It exerts numerous beneficial effects on neuroprotective, anti-inflammatory, anti-ischaemic, antimutagenic, antiviral and cardiovascular protection processes[15,16,17,18,19,20]. Statistical comparisons were performed using one-way analysis of variance. *P < 0.05, **P < 0.01 vs. sham
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