Myocardial ischemia‐reperfusion injury (MIRI) is a major cause of heart failure in patients with coronary heart disease (CHD). Mitochondrial dysfunction is the crucial factor of MIRI; oxidative stress caused by mitochondrial reactive oxygen species (ROS) aggravates myocardial cell damage through the mitochondria‐dependent apoptosis pathway. Asiatic acid (AA) is a type of pentacyclic triterpene compound purified from the traditional Chinese medicine Centella asiatica, and its protective pharmacological activities have been reported in various disease models. This study is aimed at investigating the protective effects of AA and the underlying mechanisms in MIRI. To achieve this goal, an animal model of MIRI in vivo and a cell model of oxygen‐glucose deprivation/reperfusion (OGD/R) in vitro were established. The results show that AA exerts a protective effect on MIRI by improving cardiac function and reducing cardiomyocyte damage. Due to its antioxidant properties, AA alleviates mitochondrial oxidative stress, as evidenced by the stable mitochondrial structure, maintained mitochondrial membrane potential (MMP), and reduced ROS generation, otherwise due to its antiapoptotic properties. AA inhibits the mitogen‐activated protein kinase (MAPK)/mitochondria‐dependent apoptosis pathway, as evidenced by the limited phosphorylation of p38‐MAPK and JNK‐MAPK, balanced proportion of Bcl‐2/Bax, reduced cytochrome c release, inhibition of caspase cascade, and reduced apoptosis. In conclusion, our study confirms that AA exerts cardiac‐protective effects by regulating ROS‐induced oxidative stress via the MAPK/mitochondria‐dependent apoptosis pathway; the results provide new evidence that AA may represent a potential treatment for CHD patients.

The present prospective study was conducted to investigate the independent risk and predictive value of plasma long non‑coding RNA metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) as a biomarker for the diagnosis, severity and prognosis of sepsis. A total of 120 patients with sepsis and 60 healthy controls (HCs) were recruited. The expression levels of plasma MALAT1 were detected by quantitative PCR. The results demonstrated that the plasma levels of MALAT1 were significantly increased in patients with sepsis compared with HCs (P<0.001), in patients with septic shock compared with in patients without septic shock (P<0.001), and in non‑survivors compared with in survivors (P<0.001). MALAT1 plasma levels exhibited weak positive correlation with serum procalcitonin levels (r=0.253; P=0.005), arterial lactate levels (r=0.488; P<0.001), sepsis‑related organ failure assessment scores (r=0.566; P<0.001), and acute physiology and chronic health evaluation II scores (r=0.517; P<0.001) in patients with sepsis. Multivariate logistic regression analysis revealed that high MALAT1 expression was an independent risk factor for sepsis (P<0.001), septic shock (P=0.030) and poor prognosis (P=0.015). In addition, the receiver operating characteristic curve exhibited a significant predictive value for MALAT1 in distinguishing patients with sepsis from HCs with an area under the curve (AUC) of 0.910, patients with septic shock from patients without shock with an AUC of 0.836, and non‑survivors from survivors with an AUC of 0.886. In conclusion, plasma MALAT1 may serve as a biomarker for the diagnosis, severity and prognosis of sepsis.

Asiatic acid inhibits cardiac hypertrophy by blocking interleukin- 1β-activated nuclear factor-κB signaling in vitro and in vivo