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Pinus massoniana bark extract (PMBE) is a mixture of flavonoids, and showed a capability of inducing cell apoptosis; however, its properties have not yet been fully investigated. This paper evaluates the antitumor effects of PMBE in murine sarcoma S180 both in vitro and in vivo. In vitro, the growth inhibition of S180 cells was concentration dependent on PMBE as shown by the CCK-8 assay. The AO/EB staining and flow cytometry assay showed that PMBE induced S180 cell apoptosis. Cell cycle analysis revealed that the cells in the S phase were decreased by treatment with PMBE. In vivo, the treatment of 100, 200, and 300 mg/kg PMBE reduced the tumor weight and volume of S180-bearing NIH mice by 9%-67% and 13%-68%, respectively. Peripheral leukocyte count and lymphoproliferation were increased significantly after treatment with PMBE. Our results suggest that PMBE inhibits the tumor cell growth by inducing cell apoptosis and improving lymphoproliferation. [ABSTRACT FROM AUTHOR]

Ischemic stroke is a serious health hazard that lacks effective treatment strategies. This study aims to investigate baicalin's effect on tight junctions and immune cell infiltration after ischemic stroke injury. Rat brain microvascular endothelial cells (BMECs) were treated with OGD/R to establish an in vitro model. Caspase-3, Bax, Bcl-2, zonula occludens-1 (ZO-1), occludin, claudin-5, tumor necrosis factor (TNF)- α , interleukin (IL)-6, inducible nitric oxide synthase (iNOS), Toll-like receptor (TLR) 2, TLR4, and nuclear factor-kappa B (NF- κ B) expressions were detected using qRT-PCR and western blotting. ZO-1, TNF- α , iNOS, IL6, CD31, and ZO-1 expressions were examined using immunofluorescence. A tube formation assay was performed to measure angiogenesis. An ischemia-reperfusion model in rats was established by middle cerebral artery occlusion. The infarct volume was observed using 2,3,5-triphenyltetrazolium chloride staining. TNF- α , iNOS, and IL6 levels in the serum were tested using ELISA. Flow cytometry was performed to examine immune cell inflammatory infiltration. Baicalin had no significant effect on the proliferation of normal BMECs. Baicalin inhibited apoptosis, protected against tight junction injury, and alleviated the inflammatory response in OGD/R-induced BMECs and IR rats, with the highest dose (25 μ g/mL) exerting a superior effect. Baicalin decreased the neurological function score, infarct volume, and brain water content, relieved brain morphological changes, and inhibited immune cell infiltration in vivo. In conclusion, baicalin could reduce BMECs apoptosis, protect tight junctions, and resist immune cell infiltration, thereby alleviating ischemic stroke. Our findings potentially provide a novel treatment strategy for ischemic stroke. [ABSTRACT FROM AUTHOR]

Panax ginseng is a natural medicine that has been used globally for a long time. Moreover, several studies have reported the effective activity of ginseng in treating malignancies. Various agents containing ginseng were widely used as an antitumor treatment nowadays. Lung cancer is the most common fatal cancer in China, and lung adenocarcinoma is the most common histological type of non-small cell lung cancer (NSCLC). What's worse, many patients may have a failed response to conventional therapy including chemotherapy, radiotherapy, or molecule-targeted therapy due to drug resistance. Apoptosis is a highly ordered cellular suicidal process that plays an essential role in maintaining normal homeostasis. The pharmacological mechanism of many antineoplastic drugs involves triggering of apoptotic process. In several recent studies, ginsenosides are regarded as major active components of ginseng that have the potential to control lung cancer. Most of these results have proved that ginsenosides induce apoptosis in lung cancer cells through many different signaling pathways such as PI3K/Akt, NF- κ B, EGFR, and so on. This study is aimed at reviewing the signaling pathways that underlie ginsenosides-triggered apoptotic process and encourage further studies to target promising agents against lung cancer treatment. [ABSTRACT FROM AUTHOR]

Oxidative stress has been implicated in the pathogenesis of atherosclerotic cardiovascular diseases. Dietary supplementation of anti-oxidants has been reported to have beneficial effects on the prevention of atherogenic diseases. Luteolin (a natural flavonoid) has been shown to possess antimutagenic, antitumorigenic, anti-oxidant and anti-inflammatory properties. However, the effects and underlying molecular mechanisms of luteolin on cardiovascular systems are poorly explored. Therefore, the aim of the present study was to test whether luteolin could protect against oxidative stress-induced endothelial cell injury and explore the underlying mechanisms. In this study, human umbilical vein endothelial cells (HUVECs) were pre-treated with luteolin followed by hydrogen peroxide induction (H2O2). Our results showed that luteolin protected against H2O2-induced oxidative stress and ameliorated ROS and superoxide generation. In addition, we found that luteolin treatment inhibited the H2O2-induced membrane assembly of NADPH oxidase subunits, which was further confirmed by specifically inhibiting NADPH oxidase using DPI treatment. Furthermore, pAMPK protein expression was enhanced and p-PKC isoforms were significantly down-regulated by luteolin treatment in a dose-dependent manner, and a similar effect was observed upon DPI treatment. However, co-treatment with the specific inhibitor of AMPK (Compound C) restored p-PKC levels suggesting the role of AMPK signaling in regulating p-PKC expression under oxidative stress condition in HUVECs. Finally, we confirmed using siRNAs and specific inhibitor and/or activator of AMPK (AICAR) that luteolin treatment induced AMPK is a key player and regulator of activated expression of PKC isoforms and thereby confers protection against H2O2-induced oxidative stress in HUVECs. [ABSTRACT FROM AUTHOR]

Crocin, the main effective component of saffron, exerts protective effects against ischemia/reperfusion injury during strokes. However, the effects of crocin in myocardial ischemia/reperfusion injury, and the mechanisms involved, remain unknown. Pretreated with crocin for 7 days, C57BL/6N mice were subjected to 30 min of myocardial ischemia followed by 12h of reperfusion (for cardiac function and infarct size, cell apoptosis and necrosis). Neonatal mouse cardiomyocytes were subjected to 2 h of hypoxia followed by 4 h of reoxygenation. NMCM's survival was assessed during hypoxia and reoxygenation in the presence or absence of the autophagy inhibitor 3-methyladenine or the inducer rapamycin. Western blotting was used to evaluate AMPK, Akt, and autophagy-related proteins. Autophagosome was observed using electron microscopy. In the in vivo experiment, crocin pretreatment significantly attenuated infarct size, myocardial apoptosis and necrosis, and improved left ventricular function following ischemia/reperfusion. In vitro data revealed that autophagy was induced during hypoxia, the levels of which were intensely elevated during reoxygenation. Crocin significantly promoted autophagy during ischemia, accompanied with the activation of AMPK. In contrast, crocin overtly inhibited autophagy during reperfusion, accompanied with Akt activation. Induction and inhibition of autophagy mitigated crocin induced protection against NMCMs injury during hypoxia and reoxygenation, respectively. Our data suggest that crocin demonstrated a myocardial protective effect via AMPK/mTOR and Akt/mTOR regulated autophagy against ischemia and reperfusion injury, respectively. [ABSTRACT FROM AUTHOR]