Objective. This study aimed to evaluate the protective effect of kaempferol against myocardial ischemia/reperfusion (I/R) injury in rats.Method. Left ventricular developed pressure (LVDP) and its maximum up/down rate (±dp/dtmax) were recorded as myocardial function. Infarct size was detected with 2,3,5-triphenyltetrazolium chloride staining. Cardiomyocyte apoptosis was determined using terminal deoxynucleotidyl nick-end labeling (TUNEL). The levels of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione/glutathione disulfide (GSH/GSSG) ratio, and tumor necrosis factor-alpha (TNF-α) were determined using enzyme linked immunosorbent assay (ELISA). Moreover, total glycogen synthase kinase-3β(GSK-3β), phospho-GSK-3β(P-GSK-3β), precaspase-3, cleaved caspase-3, and cytoplasm cytochrome C were assayed using Western blot analysis.Results. Pretreatment with kaempferol significantly improved the recovery of LVDP and±dp/dtmax, as well as increased the levels of SOD and P-GSK-3βand GSH/GSSG ratio. However, the pretreatment reduced myocardial infarct size and TUNEL-positive cell rate, as well as decreased the levels of cleaved caspase-3, cytoplasm cytochrome C, CK, LDH, MDA, and TNF-α.Conclusion. These results suggested that kaempferol provides cardioprotection via antioxidant activity and inhibition of GSK-3βactivity in rats with I/R.

Both phosphatidylinositol 3-kinase (PI3K)/AKT and mitogen activated protein kinase (MAPK) signaling cascades play an important role in cell proliferation, survival, angiogenesis and metastasis of tumor cells. In the present report, we investigated the effects of licochalcone A (LA), a flavonoid extracted from licorice root, on the PI3K/AKT/mTOR and MAPK activation pathways in human gastric cancer BGC-823 cells. LA increased reactive oxygen species (ROS) levels, which is associated with the induction of apoptosis as characterized by positive Annexin V binding and activation of caspase-3 and cleavage of poly-ADP-ribose polymerase (PARP). Inhibition of ROS generation by N-acetylcysteine (NAC) significantly prevented LA-induced apoptosis. Interestingly, we also observed that LA caused the activation of ERK, JNK and p38 MAPK in BGC-823 cells. The antitumour activity of LA-treated BGC-823 cells was significantly distinct in KM mice in vivo. All the findings from our study suggest that LA can interfere with MAPK signaling cascades, initiate ROS generation, induce oxidative stress and consequently cause BGC cell apoptosis.

This study aims to evaluate the cardioprotective effects of astragalin against myocardial ischemia/reperfusion (I/R) injury in isolated rat heart. The cardioprotective effects of astragalin on myocardial I/R injury were investigated on Langendorff apparatus. Adult male Sprague‐Dawley rats were randomly divided into five groups. The results showed that astragalin pretreatment improved myocardial function. Compared with I/R group, lactate dehydrogenase (LDH) and creatine kinase (CK) activities in coronary flow decreased in astragalin pretreatment groups, whereas superoxide dismutase (SOD) activity and glutathione/glutathione disulfide (GSH/GSSG) ratio significantly increased. The levels of malondialdehyde (MDA), intracellular reactive oxygen species (ROS), tumor necrosis factor‐α (TNF‐α), and interleukin‐6 (IL‐6) decreased in astragalin‐treated groups. The infarct size (IS) and apoptosis rate in hearts from astragalin‐treated groups were lower than those in hearts from the I/R group. Western blot analysis also revealed that astragalin preconditioning significantly reduced Bax level, whereas Bcl‐2 was increased in the myocardium. Therefore, astragalin exhibited cardioprotective effects via its antioxidative, antiapoptotic, and anti‐inflammatory activities.

The purpose of this study is to clarify the cardioprotective property of the aqueous extract ofElaeagnus angustifoliaL. leaf (EA) against myocardial ischemia/reperfusion injury in isolated rat heart. The myocardial ischemia/reperfusion (I/R) injury model of isolated rat heart was set up by the use of improved Langendorff retrograde perfusion technology. Compared with the ischemia/reperfusion (I/R) group, the aqueous extract ofElaeagnus angustifoliaL. leaf (0.5 mg/mL, 1.0 mg/mL) pretreatment markedly improved the coronary flow (CF) and raised left ventricular developed pressure (LVDP) and maximum rise/down velocity (±dp/dtmax). The infarct size of the EA-treated hearts was smaller than that of I/R group. After treatment with EA, the superoxide dismutase (SOD) activity increased; malondialdehyde (MDA) and protein carbonyl content reduced more obviously (P<0.01) than that of I/R injury myocardial tissue.Conclusion. Results from the present study showed that the aqueous extract ofElaeagnus angustifoliaL. leaf has obvious protective effects on myocardial I/R injury, which may be related to the improvement of myocardial oxidative stress states.