Notoginsenoside R1

Notoginsenoside R1 (NGR1) is a phytoestrogen, which can be isolated from Panax notoginseng. It is used to treat many diseases including hypoxic-ischemic injury, and it has been shown to target estrogen receptors. Endoplasmic reticulum (ER) stress plays an important role in the development of cell apoptosis during ischemia, and ER stress is known to be regulated by estrogen. However, the neuroprotective properties and underlying mechanisms of NGR1 in neonatal hypoxic-ischemic encephalopathy (HIE) and the relationship between NGR1 and ER stress is unknown. This study examined potential neuroprotective effects of NGR1 against neonatal HIE and its mechanisms. Following HIE conditions in vitro and in vivo, we administered NGR1 or the estrogen receptor inhibitor ICI-182780 and then measured cell apoptosis and brain injury. Expression of estrogen receptors α (ERα) and β (ERβ), and ER stress-associated proteins was detected by western blot upon stimulation with HIE, NGR1, or ICI-182780.

OBJECTIVE: To establish an HPLC-UV method for determining pharmacokinetic difference of notoginsenoside R1 between normal rats and ischemic rats.

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 SD rats (250-300 g), were randomly divided into 5 groups: sham, model, R1 (20 mg/kg, 40 mg/kg, 60 mg/kg). The activities of serum lactate dehydrogenase (LDH), creatine kinase (CK), myeloperoxidase (MPO), total superoxide dismutase (T-SOD), and malondialdehyde (MDA) were determined after 60 min of reperfusion. Interleukin-1β (IL-1β), interleukin-8 (IL-8) and tumor necrosis factor (TNF)-α were evaluated by enzyme-linked immunosorbent assay (ELISA), Vitamin D3 Upregulated Protein 1 (VDUP1), IκB α, P-IκB α, NF-κBP65, pNF-κBP65 were measured by western blotting. Our study demonstrated that R1 can ameliorate the impaired mitochondrial morphology and oxidation system; IL-1 β, IL-8 and TNF-α were recovered.

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 clarified. In the present study, we have evaluated the anti-inflammatory effects of NG-R1 on oxLDL-induced endothelial cells and its possible molecular mechanism of action. Our results showed that NG-R1 treatment significantly attenuated oxLDL-induced expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1β. These effects were accompanied with suppression of oxLDL-induced activation of NF-κB and Mitogen-activated protein kinases (MAPK). Moreover, NG-R1 also increased in Peroxisome proliferator-activated receptor γ (PPARγ) protein expression and transcription levels, and attenuated oxLDL-induced suppression of PPARγ expression. The inhibition of NG-R1 on oxLDL-induced TNF-α and IL-1β productions can be reversed by PPARγ antagonist GW9662.