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notoginsenoside/necrose
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Página 1 a partir de 18 resultados
Notoginsenoside R1 suppresses miR-301a via NF-κB pathway in lipopolysaccharide-treated ATDC5 cells.
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Notoginsenoside R1 inhibits oxidized low-density lipoprotein induced inflammatory cytokines production in human endothelial EA.hy926 cells.
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Notoginsenoside R1 (NG-R1), a unique and main active ingredient of Panax notoginseng, has been described to exhibit anti-inflammatory activity. However, its protective effects against oxidized low-density lipoprotein (oxLDL)-induced inflammatory injury in vascular endothelial cells have not been
Notoginsenoside R1 protects human keratinocytes HaCaT from LPS-induced inflammatory injury by downregulation of Myd88.
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Burn injury is a gigantic challenge in public health which brings multiple negative effects to patients both in physical and spiritual aspects. Inflammation plays vital roles in the progression of burn injury, and our study investigated whether notoginsenoside R1 (NGR1) alleviated lipopolysaccharide
Notoginsenoside R1 Suppresses Inflammatory Signaling and Rescues Renal Ischemia-Reperfusion Injury in Experimental Rats.
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BACKGROUND Notoginsenoside R1 (NR) is a major dynamic constituent of Panax notoginseng found to possess anti-inflammatory activity against various inflammatory diseases. However, its protective effects against renal ischemia-reperfusion (I/R) injury have not been elucidated. In male Wistar rats, we
Notoginsenoside R1 from Panax notoginseng inhibits TNF-alpha-induced PAI-1 production in human aortic smooth muscle cells.
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Notoginsenoside R1 is the main ingredient with cardiovascular activity in Panax notoginseng. We reported that notoginsenoside R1 significantly decreased tumor necrosis factor-alpha (TNF-alpha)-induced plasminogen activator inhibitor-1 (PAI-1) mRNA, protein level and secretion in human aortic smooth
Effect of notoginsenoside R1 on hepatic microcirculation disturbance induced by gut ischemia and reperfusion.
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OBJECTIVE
To assess the effect of notoginsenoside R1 on hepatic microcirculatory disturbance induced by gut ischemia/reperfusion (I/R) in mice.
METHODS
The superior mesenteric artery (SMA) of C57/BL mice was ligated for 15 min to induce gut ischemia followed by 30-min reperfusion. In another set of
Panax notoginsenoside produces neuroprotective effects in rat model of acute spinal cord ischemia-reperfusion injury.
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BACKGROUND
Acute spinal cord ischemia-reperfusion injury (SCII) is associated with pathological changes, including inflammation, edema, and neuronal apoptosis. Panax notoginsenoside (PNS), an important traditional Chinese medicine, has shown a variety of beneficial effects, including homeostasis
[Effects of Panax notoginsenoside on TNF-alpha and MMP-2 expressions in rats with post-myocardial infarction ventricular remodeling and the mechanism].
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OBJECTIVE
To observe the effects of Panax notoginsenoside (PNS) on tumor necrosis factor-alpha (TNF-alpha) and matrix metalloproteinases-2 (MMP-2) expressions in rats with post-myocardial infarction ventricular remodeling and explore the mechanism.
METHODS
Rat models of acute infarction ventricular
Notoginsenoside R1 attenuates amyloid-β-induced damage in neurons by inhibiting reactive oxygen species and modulating MAPK activation.
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Progressive accumulation of amyloid-β (Aβ) is a pathological hallmark of Alzheimer's disease (AD). Aβ increases free radical production in neuronal cells, leading to oxidative stress and cell death. An intervention that would reduce Aβ-related neurotoxicity through free radical reduction could
Protective effect of notoginsenoside R1 in a rat model of myocardial ischemia reperfusion injury by regulation of Vitamin D3 upregulated protein 1/NF-κB pathway.
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The aim of this study was to investigate the protective effects of notoginsenoside R1 (R1) in the rat model of myocardial ischemia reperfusion injury and the possible mechanisms. Myocardial ischemia/reperfusion injury (MIRI) was induced by ischemia for 30 min and reperfusion for 60 min. Fifty male
Notoginsenoside R1 alleviates TNF-α-induced pancreatic β-cell Min6 apoptosis and dysfunction through up-regulation of miR-29a.
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Diabetes mellitus (DM) is a metabolic disorder that seriously harms human health. Notoginsenoside R1 (NGR1) can be used in various diseases. We explored consequents of NGR1 on tumour necrosis factor (TNF)-α-stimulated Min6 and rat primary islets β cells. The results were that TNF-α significantly cut
Notoginsenoside Ft1 Promotes Fibroblast Proliferation via PI3K/Akt/mTOR Signaling Pathway and Benefits Wound Healing in Genetically Diabetic Mice.
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Wound healing requires the essential participation of fibroblasts, which is impaired in diabetic foot ulcers (DFU). Notoginsenoside Ft1 (Ft1), a saponin from Panax notoginseng, can enhance platelet aggregation by activating signaling network mediated through P2Y12 and induce proliferation,
Notoginsenoside R1 ameliorates podocyte injury in rats with diabetic nephropathy by activating the PI3K/Akt signaling pathway.
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The present study was designed to examine the protective effect of notoginsenoside R1 (NR1) on podocytes in a rat model of streptozotocin (STZ)‑induced diabetic nephropathy (DN), and to explore the mechanism responsible for NR1-induced renal protection. Diabetes was induced by a single injection of
Notoginsenoside R1 protects human renal proximal tubular epithelial cells from lipopolysaccharide-stimulated inflammatory damage by up-regulation of miR-26a.
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Notoginsenoside R1 protects WI-38 cells against lipopolysaccharide-triggered injury via adjusting the miR-181a/TLR4 axis.
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Notoginsenoside R1 (NGR1) is a neoteric phytoestrogen extracted from Panax notoginseng, and possesses comprehensive pharmacological functions in multitudinous ailments. But, whether NGR1 is utilized in neonatal pneumonia is not clear. This research study aspired to disclose the protective activity
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