Immunomodulatory effects of icariin in a myocardial infarction mouse model

Abstract

Myocardial infarction (MI) is a prevalent cardiovascular disease defined by myocardial ischemia and hypoxic damage caused by plaque rupture, thrombosis, lumen stenosis, or blockage in the coronary artery. However, the development of emergency percutaneous coronary interventional therapy has enabled the rapid restoration of blood perfusion to ischemic myocardium and the rescue of dying myocardium cells. Some dying myocardium cells have caused irreversible damage and impaired cardiac function recovery in recent years. Icariin has been utilized to treat various ailments as a natural chemical extract. In this study, we employed a variety of approaches to observe MI, including western blotting, quantitative RT-PCR, immunohistochemistry, and flow cytometric analysis using icariin. As demonstrated by the research findings, icariin may prevent MI-induced cell apoptosis. This is accomplished by inhibiting proinflammatory factors via the Nrf2/HO-1 signaling pathways. These data imply that icariin may be an effective treatment for MI.

Keywords: Icariin; immune response; inflammatory; myocardial infarction; nrf2/HO-1.

Graphical abstract

Figure 1.

Icariin improves cardiac function after myocardial infarction: (a) Thoracic echocardiography of mice after 28 days of treatment compared to the sham group. (b) Illustration of H&E staining and measurement of the cross-sectional area of the fibers in the hearts (× 100). (c) Digitalized slides of Masson’s trichrome-stained heart paraffin slices and collagen volume. Collagen has been dyed in blue, and the cytoplasm has been stained in red, respectively (× 100).

Figure 2.

Icariin prevents myocardial cell apoptosis: (a) Mice myocardial were stained with TUNEL, *P < 0.05. (b) The protein expression of Bcl-2, Bax, cytochrome c, cleaved caspase-3, and GAPDH (control) were determined by Western blotting. Each experience was repeated 3 times *P < 0.05.

Figure 3.

Icariin improves mice immune system: Flow cytometric analysis was performed to assess the population of lymphocytes (CD8+ CTL cells and CD3+ CD4++IFN-γ+ Th1) in the spleen and heart.

Figure 4.

Icariin promotes activation of Nrf2/HO-1 by alleviating inflammatory factors. Signaling pathways: (a) Immunohistochemical was performed to check the expression of IL-17 (× 100); the experiment was repeated 3 times with means *P < 0.05. (b) qPCR was performed to evaluate the mRNA expression of IL1β, HO-1, TNF-α, and α-SMA compared to 18S. Each experience was repeated 3 times *P < 0.05. (c) The protein expression of HO-1, Nrf2, and GAPDH (control) was determined by Western blotting. Each experience was repeated 3 times *P < 0.05.

Figure 5.

Molecular mechanism by which Icariin induces myocardial cell protection.