Red emissive carbon dots (CDs) have drawn more and more attention due to their good organ penetration depth and slight biological tissue photodamage. Herein, the fluorescent CDs with red emission were synthesized by the facile one-pot hydrothermal treatment of citric acid and neutral red and they show red fluorescence both in aqueous solution and solid state. The solution of CDs exhibits the quantum yield of 12.1%, good stability against photobleaching, and low cytotoxicity. As-prepared CDs can be used as a fluorescent probe for peculiar detection of Pt, Au, and Pd. Furthermore, the CDs show excellent biocompatibility, which were successfully used as hopeful bioimaging and biosensing of noble metal ions in PC12 cells and zebrafish.
Aim: Berberine (BBR), an isoquinoline-derived alkaloid isolated from Rhizoma coptidis, exerts cardioprotective effects. Because endoplasmic reticulum (ER) stress plays a pivotal role in myocardial ischemia/reperfusion (MI/R)-induced apoptosis, it was interesting to examine whether the protective effects of BBR resulted from modulating ER stress levels during MI/R injury, and to define the signaling mechanisms in this process. Methods: Male rats were treated with BBR (200 mg·kg -1 ·d -1 , ig) for 2 weeks, and then subjected to MI/R surgery. Cardiac dimensions and function were assessed using echocardiography. Myocardial infarct size and apoptosis was examined. Total serum LDH levels and CK activities, superoxide production, MDA levels and the antioxidant SOD activities in heart tissue were determined. An in vitro study was performed on cultured rat embryonic myocardium-derived cells H9C2 exposed to simulated ischemia/reperfusion (SIR). The expression of apoptotic, ER stress-related and signaling proteins were assessed using Western blot analyses. Results: Pretreatment with BBR significantly reduced MI/R-induced myocardial infarct size, improved cardiac function, and suppressed myocardial apoptosis and oxidative damage. Furthermore, pretreatment with BBR suppressed MI/R-induced ER stress, evidenced by down-regulating the phosphorylation levels of myocardial PERK and eIF2α and the expression of ATF4 and CHOP in heart tissues. Pretreatment with BBR also activated the JAK2/STAT3 signaling pathway in heart tissues, and co-treatment with AG490, a specific JAK2/STAT3 inhibitor, blocked not only the protective effects of BBR, but also the inhibition of BBR on MI/R-induced ER stress. In H9C2 cells, treatment with BBR (50 μmol/L) markedly reduced SIR-induced cell apoptosis, oxidative stress and ER stress, which were abolished by transfection with JAK2 siRNA. Conclusion: BBR ameliorates MI/R injury in rats by activating the AK2/STAT3 signaling pathway and attenuating ER stress-induced apoptosis.Keywords: berberine; myocardial ischemia/reperfusion injury; apoptosis; ER stress; oxidative stress; JAK2/STAT3; AG490 Acta Pharmacologica Sinica (2016) 37: 354-367; doi: 10.1038/aps.2015 published online 25 Jan 2016 Original Article # These authors contributed equally to this work. * To whom correspondence should be addressed. E-mail yunwangww@163.com (Yun WANG);shiqiangyu210@126.com (Shi-qiang YU) Received 2015-08-26 Accepted 2015-11-20 IntroductionIschemic heart disease remains the leading cause of mortality and disability worldwide. Although timely reperfusion therapy is the primary treatment, reperfusion itself results in major cardiac damage, commonly referred to as myocardial ischemia/reperfusion (MI/R) injury [1,2] . The endoplasmic reticulum (ER) is a multifunctional organelle in eukaryotic cells, which participates in the biosynthesis and folding of proteins. MI/R injury is known to result in the accumulation of unfolded proteins in the ER, which causes a severe unfolded protein response (UPR). Persistent UPR eventually ...
Propofol infusion syndrome (PRIS) is an uncommon life-threatening complication observed most often in patients receiving high-dose propofol. High-dose propofol treatment with a prolonged duration can damage the immune system. However, the associated molecular mechanisms remain unclear. An increasing number of clinical and experimental observations have demonstrated that tissue-resident macrophages play a critical role in immune regulation during anaesthesia and procedural sedation. Since the inflammatory response is essential for mediating propofol-induced cell death and proinflammatory reactions, we hypothesised that propofol overdose induces macrophage pyroptosis through inflammasomes. Using primary cultured bone marrow-derived macrophages, murine macrophage cell lines (RAW264.7, RAW-asc and J774) and a mouse model, we investigated the role of NLRP3 inflammasome activation and secondary pyroptosis in propofol-induced cell death. We found that high-dose propofol strongly cleaved caspase-1 but not caspase-11 and biosynthesis of downstream interleukin (IL)-1β and IL-18. Inhibition of caspase-1 activity blocks IL-1β production. Moreover, NLRP3 deletion moderately suppressed cleaved caspase-1 as well as the proportion of pyroptosis, while levels of AIM2 were increased, triggering a compensatory pathway to pyroptosis in NLRP3 -/- macrophages. Here, we show that propofol-induced mitochondrial reactive oxygen species (ROS) can trigger NLRP3 inflammasome activation. Furthermore, apoptosis-associated speck-like protein (ASC) was found to mediate NLRP3 and AIM2 signalling and contribute to propofol-induced macrophage pyroptosis. In addition, our work shows that propofol-induced apoptotic initiator caspase (caspase-9) subsequently cleaved effector caspases (caspase-3 and 7), indicating that both apoptotic and pyroptotic cellular death pathways are activated after propofol exposure. Our studies suggest, for the first time, that propofol-induced pyroptosis might be restricted to macrophage through an NLRP3/ASC/caspase-1 pathway, which provides potential targets for limiting adverse reactions during propofol application. These findings demonstrate that propofol overdose can trigger cell death through caspase-1 activation and offer new insights into the use of anaesthetic drugs.
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