Background. Vaspin is an important adipokine that is involved in cardiovascular diseases. This study is aimed at investigating whether vaspin participates in sepsis-induced cardiac injury and explored the possible mechanism. Methods. First, cecal ligation and puncture (CLP) and lipopolysaccharide (LPS) were used to establish a mouse model of sepsis, and cardiac vaspin expression was examined. In addition, after pretreatment with vaspin or phosphate-buffered saline (PBS), wild-type (WT) mice underwent CLP to establish a septic model and received sham as a control. Finally, WT mice and kallikrein 7 (KLK7-/-) mice were underwent CLP with or without vaspin pretreatment. Results. Mice that underwent CLP and were administered LPS exhibited increased vaspin expression in both the heart and serum compared with sham- or saline-treated mice. In CLP mice, pretreatment with vaspin reduced mortality and alleviated the expression of cardiac injury markers and cardiac dysfunction. In addition, vaspin reduced the cardiac levels of CD45+ cells and CD68+ cells, alleviated the cardiac inflammatory response, and reduced cardiomyocyte apoptosis. The protective effects of vaspin on CLP mice were masked by the deletion of KLK7, which was demonstrated to be a downstream signal of vaspin. Conclusions. Vaspin alleviates cardiac inflammation and plays a protective role in sepsis-induced cardiac injury by reducing KLK7 expression.

Previous studies showed that interleukin‐9 (IL‐9) is involved in cardiovascular diseases, including hypertension and cardiac fibrosis. This study aimed to investigate the role of IL‐9 in lipopolysaccharide (LPS)‐induced myocardial cell (MC) apoptosis. Mice were treated with LPS, and IL‐9 expression was measured and the results showed that compared with WT mice, LPS‐treated mice exhibited increased cardiac Mø‐derived IL‐9. Additionally, the effects of IL‐9 deficiency (IL‐9−/−) on macrophage (Mø)‐related oxidative stress and MC apoptosis were evaluated, the results showed that IL‐9 knockout significantly exacerbated cardiac dysfunction, inhibited Nrf2 nuclear transfer, promoted an imbalance in M1 and M2 Møs, and exacerbated oxidative stress and MC apoptosis in LPS‐treated mice. Treatment with ML385, a specific nuclear factor erythroid‐2 related factor 2 (Nrf2) pathway inhibitor significantly alleviated the above effects in LPS‐treated IL‐9−/− mice. Bone marrow‐derived Møs from wild‐type (WT) mice and IL‐9−/− mice were treated with LPS, and the differentiation and oxidative stress levels of Møs were measured. The effect of Mø differentiation on mouse MC apoptosis was also analyzed in vitro. The results showed that LPS‐induced M1 Mø/M2 Mø imbalance and Mø‐related oxidative stress were alleviated by IL‐9 knockout but were exacerbated by ML385 treatment. The protective effects of IL‐9 deficiency on the MC apoptosis mediated by LPS‐treated Møs were reversed by ML‐385. Our results suggest that deletion of IL‐9 decreased the nuclear translocation of Nrf2 in Møs, which further aggravated Mø‐related oxidative stress and MC apoptosis. IL‐9 may be a target for the prevention of LPS‐induced cardiac injury.