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article, google, scholar, cas, pyroptosis, cell, salidroside, atherosclerosis, endothelial, yang, wang, sal, chengdu, zhang, chen, journal, research, inflammation, cells, inflammasome, university, nlrp, liu, death, access, pathway, china, privacy, cookies, content, inhibiting, xing, international, shi, nature, attenuates, cellular, sichuan, hospital, peoples, republic, xss, data, information, publish, search, plaque, published, jin, activation,

Topics {✒️}

mitochondria-related ampk/pi3k/akt/enos pathway regulating pi3k/pkb/nrf2/nfkappab signaling ampk-dependent txnip/nlrp3 pathway ros/nlrp3/caspase-1 signaling pathway hypoxia-inducible factor-1alpha expression lps-induced inflammatory injury high-fat diet month download article/chapter txnip-nlrp3 inflammasome pathway phosphatidylinositol 3-kinase/protein kinase cell death research human umbilical cords atherosclerosis-related pyroptosis salidroside reduces inflammation il-1β induced related subjects atherosclerosis-related inflammation sirt1-dependent inhibition privacy choices/manage cookies full article pdf article inflammation aims nlrp3 inflammasome activation ki mice fed dying eukaryotic cells laboratory animals published yu-ting yang wen-jing li exert anti-oxidative inhibiting caspase-1 activation european economic area article xing anti-inflammatory properties animal ethics committee endothelial cells atherosclerotic plaque tunel-positive staining clinica chimica acta forming membrane pores complement c3 activity evidence-based complementary extracellular matrix accumulation chemico-biological interactions 278 interleukin-1beta secretion cell research 25 cell death atherosclerosis mouse model nicotine promotes atherosclerosis conditions privacy policy anti-atherosclerotic effects sal anti-inflammatory

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         headline:Salidroside Decreases Atherosclerosis Plaque Formation via Inhibiting Endothelial Cell Pyroptosis
         description:Pyroptosis, a new pro-inflammatory programmed cell death, is linked to atherosclerosis (AS). Our previous studies suggested that salidroside (SAL) can alleviate AS and exert anti-oxidative and anti-inflammatory properties. However, the effect of SAL on atherosclerosis-related pyroptosis has not been studied. Here, we investigated the effect of SAL on pyroptosis to explain the underlying mechanisms of SAL on atherosclerosis-related inflammation. We established an atherosclerosis mouse model via western diet (HFD) to explore the protective effect of SAL. According to our results, administration of SAL for 12 weeks markedly reduced the atherosclerotic plaque in aorta. Meanwhile, SAL also alleviated the pyroptosis, as evidenced by inhibiting caspase-1 activation, interleukin-1β (IL-1β) release, and TUNEL-positive staining, and decreasing the expression of Gasdermin D (GSDMD). Furthermore, SAL also decreased the activation of caspase-1 and inhibited the release of IL-1β induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP) in human umbilical vein endothelial cell (HUVECs). Our data indicate that SAL inhibit NLRP3-related pyroptosis, which might be the underlying mechanism of SAL anti-inflammatory in atherosclerosis.
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      headline:Salidroside Decreases Atherosclerosis Plaque Formation via Inhibiting Endothelial Cell Pyroptosis
      description:Pyroptosis, a new pro-inflammatory programmed cell death, is linked to atherosclerosis (AS). Our previous studies suggested that salidroside (SAL) can alleviate AS and exert anti-oxidative and anti-inflammatory properties. However, the effect of SAL on atherosclerosis-related pyroptosis has not been studied. Here, we investigated the effect of SAL on pyroptosis to explain the underlying mechanisms of SAL on atherosclerosis-related inflammation. We established an atherosclerosis mouse model via western diet (HFD) to explore the protective effect of SAL. According to our results, administration of SAL for 12 weeks markedly reduced the atherosclerotic plaque in aorta. Meanwhile, SAL also alleviated the pyroptosis, as evidenced by inhibiting caspase-1 activation, interleukin-1β (IL-1β) release, and TUNEL-positive staining, and decreasing the expression of Gasdermin D (GSDMD). Furthermore, SAL also decreased the activation of caspase-1 and inhibited the release of IL-1β induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP) in human umbilical vein endothelial cell (HUVECs). Our data indicate that SAL inhibit NLRP3-related pyroptosis, which might be the underlying mechanism of SAL anti-inflammatory in atherosclerosis.
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