S Fan1, J-B Sun, R Li, X Song, J Li. 1. Department of Pharmacy, Emergency General Hospital, Beijing, China. lijing0127650@163.com.
Abstract
OBJECTIVE: The aim of this research was to explore the protective effect of lycopene (Lyc) on myocardial ischemia injury through anti-apoptosis and anti-oxidative stress. MATERIALS AND METHODS: 75 rats were divided into 5 groups: sham operation group (control group), model group, low-dose group (Lyc+2 mg/kg), medium-dose group (Lyc+4 mg/kg) and high-dose group (Lyc+6 mg/kg). The rat model of myocardial ischemia was established by a subcutaneous injection of isoproterenol (85 mg/kg) for two consecutive days. Conventional HE staining and Masson staining were performed for pathological changes. Biochemical indicators were measured by the enzyme-linked immuno sorbent assay (ELISA). Western blotting was used to measure the levels of related proteins in JNK/STAT signaling pathway. RESULTS: Compared to control group, the levels of CK-MB, TC, and TGs were significantly increased in model group. The levels of CK-MB, TC, and TGs in each Lyc-administered group were decreased. After Lyc was administered, the SOD, CAT, GSH-Px activities and MDA content were all restored. The serum levels of IL-1β, TNF-α and IL-6 in control group were significantly lower than in model group. When the Lyc was administered, the serum IL-1β, TNF-α and IL-6 levels in medium-dose group and high-dose group were significantly decreased. The levels of Bax/Bcl-2, Cyt-c, and Caspase-3 in model group were significantly higher than control group. Changes of Bax/Bcl-2, Cyt-c, and Caspase-3 in medium-dose and high-dose groups after the administration of Lyc were restored significantly. The levels of p-JNK/JNK, p-STAT1 (Tyr701)/STAT1, p-STAT1 (Ser727)/STAT1, p-STAT3 (Tyr705)/STAT3 were significantly increased, while p-STAT3 (Ser727)/STAT3 was significantly decreased. When Lyc was administered, the expression levels of p-JAK/JAK, p-STAT1 (Tyr701)/STAT1, p-STAT1 (Ser727)/STAT1, p-STAT3 (Tyr705)/STAT3 protein in medium-dose group and high-dose group were significantly decreased, and the expression level of p-STAT3 (Ser727)/STAT3 protein was significantly increased. CONCLUSIONS: Lyc could show a protective effect on oxidative stress injury and anti-cardiomyocyte apoptosis of myocardial ischemia, and its possible mechanism was to attenuate the activation of JNK/ERK signaling pathway induced by myocardial injury.
OBJECTIVE: The aim of this research was to explore the protective effect of lycopene (Lyc) on myocardial ischemia injury through anti-apoptosis and anti-oxidative stress. MATERIALS AND METHODS: 75 rats were divided into 5 groups: sham operation group (control group), model group, low-dose group (Lyc+2 mg/kg), medium-dose group (Lyc+4 mg/kg) and high-dose group (Lyc+6 mg/kg). The rat model of myocardial ischemia was established by a subcutaneous injection of isoproterenol (85 mg/kg) for two consecutive days. Conventional HE staining and Masson staining were performed for pathological changes. Biochemical indicators were measured by the enzyme-linked immuno sorbent assay (ELISA). Western blotting was used to measure the levels of related proteins in JNK/STAT signaling pathway. RESULTS: Compared to control group, the levels of CK-MB, TC, and TGs were significantly increased in model group. The levels of CK-MB, TC, and TGs in each Lyc-administered group were decreased. After Lyc was administered, the SOD, CAT, GSH-Px activities and MDA content were all restored. The serum levels of IL-1β, TNF-α and IL-6 in control group were significantly lower than in model group. When the Lyc was administered, the serum IL-1β, TNF-α and IL-6 levels in medium-dose group and high-dose group were significantly decreased. The levels of Bax/Bcl-2, Cyt-c, and Caspase-3 in model group were significantly higher than control group. Changes of Bax/Bcl-2, Cyt-c, and Caspase-3 in medium-dose and high-dose groups after the administration of Lyc were restored significantly. The levels of p-JNK/JNK, p-STAT1 (Tyr701)/STAT1, p-STAT1 (Ser727)/STAT1, p-STAT3 (Tyr705)/STAT3 were significantly increased, while p-STAT3 (Ser727)/STAT3 was significantly decreased. When Lyc was administered, the expression levels of p-JAK/JAK, p-STAT1 (Tyr701)/STAT1, p-STAT1 (Ser727)/STAT1, p-STAT3 (Tyr705)/STAT3 protein in medium-dose group and high-dose group were significantly decreased, and the expression level of p-STAT3 (Ser727)/STAT3 protein was significantly increased. CONCLUSIONS:Lyc could show a protective effect on oxidative stress injury and anti-cardiomyocyte apoptosis of myocardial ischemia, and its possible mechanism was to attenuate the activation of JNK/ERK signaling pathway induced by myocardial injury.