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Effects of Xinjierkang on Nrf2/HO-1 expression in viral myocarditis mice models
Jie Yin1, Wencheng Li1, Weidong Yao2
1Department of Cardiology ，Jinan people's Hospital，jinan，shandong，271100，China.
Abstract:
In this study, the changes of Nrf2/HO-1 and cytokines TNF-α, IL-6, IL-17 and IL-1β in cardiac muscle cells of Viral myocarditis (VMC) mice were detected in order to clarify the mechanism of action of Xinjierkang (XJEK). One hundred and fifty healthy male BALBC mice were randomly divided into the normal group, model group, low-, medium- and high-dose XJEK groups, with 30 in each group. Replication of the VMC model in mice inoculated with CVB3m. Serum inflammatory factors TNF-α, IL-6, IL-17 and IL-1β, Nrf2 and HO-1 protein levels in myocardial tissue were compared. The results showed that no apoptotic cells were found in the myocardium of normal mice. The percentage of cardiomyocyte apoptosis in the low, medium and high dose groups of XJEK was significantly lower than the model group (P <0.05). At 3, 7, 14, 21, and 28 days after inoculation, compared with the normal group, the TNF-α, IL-6, IL-17 and IL-1β levels in the model group significantly increased (p < 0.05). After the administration of XJEK, compared with the model group, the TNF-α, IL-6, IL-17, and IL-1β levels in the low-, middle-, and high-dose XJEK groups significantly decreased (p < 0.05). At 28 days after inoculation, compared with the normal group, the expressions of Nrf2 and HO-1 proteins in the myocardial tissue of the model group were significantly down-regulated (p < 0.05); and compared with the model group, the expressions of Nrf2 and HO-1 proteins in the low-, medium-, and high-dose XJEK groups were significantly up-regulated (p < 0.05) in a concentration-dependent manner. In conclusion, XJEK can prevent myocardial injury in VMC mice, and its mechanism of action may be related to improving myocardial cell apoptosis, inhibiting inflammatory response, and up-regulating the expression of Nrf2 and HO-1 proteins in myocardial tissue.
Insights
Xinjierkang (XJEK) treatment significantly reduced cardiomyocyte apoptosis and inflammation in viral myocarditis (VMC) mice. It also upregulated Nrf2 and HO-1 protein expression, suggesting a protective effect against myocardial injury.
Area of Science:
- Cardiology
- Immunology
- Pharmacology
Background:
- Viral myocarditis (VMC) is a serious cardiac condition often leading to myocardial injury.
- Understanding the molecular mechanisms underlying VMC and identifying effective therapeutic interventions are critical.
Purpose of the Study:
- To investigate the therapeutic effects of Xinjierkang (XJEK) on viral myocarditis in a mouse model.
- To elucidate the potential mechanisms of XJEK action, focusing on the Nrf2/HO-1 pathway and inflammatory cytokines.
Main Methods:
- Viral myocarditis was induced in BALBC mice using CVB3.
- Mice were randomly assigned to normal, model, or varying doses of XJEK treatment groups.
- Levels of inflammatory cytokines (TNF-α, IL-6, IL-17, IL-1β) and protein expression of Nrf2 and HO-1 in myocardial tissue were assessed.
Main Results:
- XJEK treatment significantly reduced cardiomyocyte apoptosis compared to the model group.
- XJEK administration led to a significant decrease in elevated levels of TNF-α, IL-6, IL-17, and IL-1β.
- Expression of Nrf2 and HO-1 proteins in myocardial tissue was significantly upregulated by XJEK in a dose-dependent manner.
Conclusions:
- Xinjierkang demonstrates protective effects against myocardial injury in viral myocarditis.
- XJEK's mechanism involves mitigating cardiomyocyte apoptosis, suppressing inflammatory responses, and enhancing Nrf2/HO-1 protein expression in the heart.
