Background: Myocardial ischemia/reperfusion (I/R) injury has become a global public health concern.An increasing amount of evidence has shown that polyphyllin I (PPI) has anti-apoptotic and antioxidant functions. This study was performed to evaluate the cardioprotective effects of PPI in a rat model of myocardial I/R injury and the underlying mechanism. Methods:We exposed induced a rat model of I/R injury by exposing rat hearts to left anterior descending coronary artery ligation for 30 min, followed by 24 h of reperfusion. Cardiac function was analyzed by echocardiography and HE staining. Myocardial apoptosis, inflammation, and oxidative stress were detected to analyze the PPI's role in I/R injury. Results:The results showed that pretreatment with PPI improved impaired histological morphology, as shown by histopathological examination. Echocardiography analysis showed that PPI increased the levels of HR, left ventricular ejection fraction (LVEF), and left ventricular wall thickness (LVWT), accompanied by decreased left ventricular end-systolic volume (LVESV). Also, PPI decreased the expression of CK-MB, Mb, cTnI, and LDH. Specifically, PPI also changed the expression of apoptotic makers (Caspase-3, Bax, and Bcl-2), inflammatory cytokines (TNF-α, IL-6, iNOS, and IL-10) and oxidative stress markers (SOD, GSH, ROS, and MDA). Notably, western blot (WB) showed that PPI treatment inhibited the phosphorylation activity of NF-κB p65. Conclusions:The findings showed that PPI exerted a favorable protective effect on I/R injury by inhibiting the inflammatory response and oxidative stress. It offered new drug candidates for the treatment of myocardial I/R injury.

Background: Prediabetes has been related with increased risk of coronary artery disease (CAD). However, the prognostic efficacy of prediabetes for patients receiving percutaneous coronary intervention (PCI) remains undetermined. We aimed to quantitatively evaluate the influence of diabetes on the risks of major adverse cardiovascular events (MACEs) after PCI in a meta-analysis. Methods: Longitudinal follow-up studies evaluating the association between prediabetes and risks of MACEs and mortality after PCI were identified by search of PubMed and Embase databases. A random-effect model was applied to pool the results. Subgroup analyses were performed to evaluate the impacts of study characteristics on the outcome. Results: Twelve follow-up studies including 10,048 patients that underwent PCI were included. Compared with patients with normoglycemia at admission, those with prediabetes were had significantly higher risk MACEs during follow-up (adjusted risk ratio [RR]: 1.53, 95% confidence interval [CI]: 1.25–1.87, P < 0.001). Further subgroup analyses indicated that the association between prediabetes and higher risk of MACEs remained regardless of the study design, sample size, CAD subtype, PCI type, definition of diabetes, or follow-up duration. Moreover, patients with prediabetes had higher significantly risk of MACEs in studies with adjustment of coronary lesion severity (RR: 1.79, P < 0.001), but the association became insignificant in studies without adjustment of the coronary lesion severity (RR: 1.23, P = 0.09). Conclusions: Prediabetes is independently associated with increased risk of MACEs after PCI as compared with those with normoglycemia, even in studies with adjustment of coronary severity.

Coronary microembolization (CME) is a prevalent cardiovascular disease, especially nowadays when percutaneous coronary intervention is widely applied. However, neither cardio-protective agents nor devices for distal protection could effectively prevent the occurrence of CME. Therefore, we aimed to develop a new drug for CME. Rats were orally administrated with different doses of Cryptotanshinone (CTS, 5, 15, 45 mg/ kg) daily for 2 weeks, respectively, following CME surgery. Then cardiac function and cardiac injury were evaluated in CME rats as well as measuring oxidative stress and apoptosis in cardiomyocytes. Compared to sham group, CME operation induced cardiac dysfunction, cardiac injury, the activation of platelet and endothelium, cardiomyocyte apoptosis and oxidative stress, all of which could be dose-dependently restored by CTS pretreatment. Moreover, NF-κB signaling pathway participated in the development of CME and also in the preventive process of CTS against CME. CTS might serve as a potential and promising candidate drug to prevent the occurrence of CME.

<b><i>Background:</i></b> Oxidative stress is a key factor that results in cardiomyocyte apoptosis and cardiovascular diseases. Cryptotanshinone (CTS), one of the major bioactive constitutes extracted from the root of the plant <i>Salvia miltiorrhiza</i>Bunge, has been widely studied for various disease treatments. However, the roles of CTS on cardiomyocytes remain unclear. <b><i>Methods:</i></b> In the present study, neonatal rat cardiomyocytes were pretreated with CTS for 4 h before being exposed to H₂O₂. Cell viability for the cells with or without pretreatment with CTS before exposure to H₂O₂ was evaluated by the MTT assay. Production of lactate dehydrogenase (LDH), nitric oxide (NO), prostaglandin E₂ (PGE₂), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxides (GSH-Px) was quantified by corresponding detection kits. The mRNA levels of Bcl-2 antiapoptotic and Bax-like proapoptotic genes were quantified with RT-PCR. Production of reactive oxygen species (ROS) was qualified and quantified with a dichlorofluorescein diacetate cellular ROS detection assay kit. The extracellular signal-related kinase (ERK) phosphorylation and nuclear factor κB (NF-κB) activation were measured by Western blot. <b><i>Results:</i></b> Our results revealed that the CTS pretreatment could enhance cell viability and promote Bcl-2 antiapoptotic gene expression. Additionally, CTS could abolish the H₂O₂-induced production of NO, LDH, and PGE₂. Consistent with these findings, CTS could inhibit ROS and MDA production and promote SOD, CAT, and GSH-Px activities. Mechanistically, CTS may achieve these processes by inhibiting ERK and NF-κB signal pathways. <b><i>Conclusion:</i></b> CTS protects cardiomyocytes against the H₂O₂-induced cellular injuries through ERK and NF-κB inactivation and ROS scavenging. Therefore, CTS is a promising reagent against ROS-induced cardiomyopathy.