Effects Of Panax Notoginseng Saponins Research Articles

Panax notoginseng saponins ameliorates experimental hepatic fibrosis and hepatic stellate cell proliferation by inhibiting the Jak2/Stat3 pathways

ObjectiveTo investigate the inhibitory effect of Panax notoginseng saponins (PNS) on liver fibrosis and explore the underlying mechanisms. MethodsCarbon tetrachloride (CCl4)-treated rats and hepatic stellate cells (HSCs) were used. The effect of PNS on CCl4-induced liver fibrosis was studied with histochemical and biochemical analysis. Transforming growth factor (TGF)-β1, α-smooth muscle actin (α-SMA), and collagen I mRNA expression were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Meanwhile, the protein expression levels of α-SMA, collagen I, phosphorylation-Janus activated kinase signal transducer (p-Jak2) / Jak2, and phosphorylation-activator of transcription (p-Stat)3 / Stat3 were determined by immunohistochemistry and / or immunoblotting. ResultsPNS treatment significantly improved the liver function of rats as indicated by decreased serum enzymatic activities of alanine aminotransferase and aspartate aminotransferase. Histopathological results indicated that PNS alleviated liver damage and reduced the formation of fibrous septa. Moreover, PNS significantly decreased liver hydroxyproline and significantly attenuated expressions of collagen I, α-SMA, TGF-β1, p-Jak2 / Jak2, and p-Stat3 / Stat3 in the rat liver fibrosis model and HSCs. ConclusionPNS can relieve liver fibrosis by modulating Jak2/Stat3 signaling transduction pathway, which may be one of its mechanisms to suppress hepatic fibrosis.

Effects of Panax notoginseng saponins on proliferation and differentiation of rat embryonic cortical neural stem cells

BackgroundWe aimed to study the effect of Panax notoginseng saponins (PNS) on the proliferation, differentiation, self-renewal, and expressions of basic fibroblast growth factor (bFGF) and brain-derived neurotrophic factor (BDNF) in rat embryonic neural stem cells (NSCs). MethodsCortical stem cells were isolated from rat embryos on Embryonic Day 17 (E17) and identified by nestin expression. Subsequently, primary culture, subculturing, and single cell cloning were performed on the cells. After the first cell passage (P1), the cells were resuspended and divided into a control group and a treatment group. Control cells were cultured in serum-free basal culture medium with B27 and dulbecco's modified eagle medium (DMEM)/F12. The same medium supplemented with PNS (100 μg/mL) was used to culture cells in the treatment group. Both groups were incubated at 37°C in a 5% CO2 incubator. Immunocytochemistry was performed 4 days after incubation. ResultsPrimary, P1, and P2 cells in the treatment group formed neurospheres, as did single cell clones of the P1 cells in this group. After being cultured for 4 days, the number of nestin-, proliferating cell nuclear antigen (PCNA)-, Tuj-1-, neurofilament (NF)-, vimentin-, glial fibrillary acidic protein (GFAP)-, bFGF-, and BDNF-positive cells significantly increased in the treatment group in comparison to the control group. All positively stained cells could form clear clusters. ConclusionPNS can promote rat embryonic cortical NSC survival, self-renewal, proliferation, and differentiation through neurotrophic factors by autocrine or paracrine signaling.

Effect of Panax NotoginSeng Saponins on motor evoked potentials of spinal cord injured rats with motion function

To investigate the effect of Panax NotoginSeng Saponins(PNS) on functional recovery of rats with spinal cord injury (SCI) after exercise. SD normal rats were randomly divided into normal control group (Normal) and control group (Sham), spinal cord injury (SCI) and spinal cord injury (SCI) + panax notoginseng saponins group (PNS) (n=8). All rats were given basso beattie bresnahan motor function score (BBB) and motor evoked potentials (MEP) examination to observe rat hind limb motor function recovery before operation and 1,3,7,14,21,28 days after operation. After operation, the BBB scores of Sham group, PNS group, SCI group were lower than that of normal; MEP amplitude was lower than that of normal group; the incubation time was prolonged compared with that in normal group. In PNS group compared with that in the SCI group, BBB scores at 7,14,21 and 28 days was significantly different(P<0.05). There were significant differences in the latency (Lat) and amplitude(Amp) of MEP within PNA subgroups or between the PNS and the SCI groups at 7,14,21,28 days(P<0.05). PNS can promote the recovery of motor function after SCI in rats.

Protective Effects of Panax notoginseng Saponins against High Glucose-Induced Oxidative Injury in Rat Retinal Capillary Endothelial Cells.

Diabetic retinopathy, a leading cause of visual loss and blindness, is characterized by microvascular dysfunction. Hyperglycemia is considered the major pathogenic factor for diabetic retinopathy and is associated with increased oxidative stress in the retina. In this study, we investigated the potential protective effects of Panax notoginseng Saponins (PNS) in retinal capillary endothelial cells (RCECs) exposed to high glucose conditions. We found a pronounced increase in cell viability in rat RCECs incubated with both PNS and high glucose (30 mM) for 48 h or 72 h. The increased viability was accompanied by reduced intracellular hydrogen peroxide (H2O2) and superoxide (O2 −), decreased mitochondrial reactive oxygen species (ROS), and lowered malondialdehyde (MDA) levels. PNS also increased the activities of total superoxide dismutase (SOD), MnSOD, catalase (CAT), and glutathione peroxidase (GSH-PX). The glutathione (GSH) content also increased after PNS treatment. Furthermore, PNS reduced NADPH oxidase 4 (Nox4) expression. These results indicate that PNS exerts a protective effect against high glucose-induced injury in RCECs, which may be partially attributed to its antioxidative function.

Panax notoginseng saponins protect kidney from diabetes by up-regulating silent information regulator 1 and activating antioxidant proteins in rats.

To explore the mechanism of the protective effects of Panax notoginseng saponins (PNS) on kidney in diabetic rats. Diabetic rat model was obtained by intravenous injection of alloxan, and the rats were divided into model, PNS-100 mg/(kg day) and PNS-200 mg/(kg day) groups, 10 each. Another 10 rats injected with saline were served as control. Periodic acid-Schiff staining and immunological histological chemistry were used to observe histomorphology and tissue expression of bone morphogenetic protein-7 (BMP-7). Silent information regulator 1 (SIRT1) was silenced in rat mesangial cells by RNA interference. The mRNA expressions of SIRT-1, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor β1 (TGF-β1) and plasminogen activator inhibitor-1 (PAI-1) were analyzed by reverse transcription polymerase chain reaction. The protein expressions of SIRT1 and the acetylation of nuclear factor κB (NF-κB) P65 were determined by western blotting. The concentration of MCP-1, TGF-β1 and malondialdehyde (MDA) in culture supernatant were detected by enzyme-linked immuno sorbent assay. The activity of superoxide dismutase (SOD) was detected by the classical method of nitrogen and blue four. In diabetic model rats, PNS could not only reduce blood glucose and lipid (P<0.01), but also increase protein level of BMP-7 and inhibit PAI-1 expression for suppressing fibrosis of the kidney. In rat mesangial cells, PNS could up-regulate the expression of SIRT1 (P<0.01) and in turn suppress the transcription of TGF-β1 (P<0.05) and MCP-1 (P<0.05). PNS could also reverse the increased acetylation of NF-κB p65 by high glucose. In addition, redox regulation factor MDA was down-regulated (P<0.05) and SOD was up-regulated (P<0.01), which were both induced by SIRT1 up-regulation. PNS could protect kidney from diabetes with the possible mechanism of up-regulating SIRT1, therefore inhibiting inflammation through decreasing the induction of inflammatory cytokines and TGF-β1, as well as activating antioxidant proteins.

Inhibitory effect of Panax notoginseng saponins on alveolar epithelial to mesenchymal transition

In the study, the effects of Panax notoginseng saponins (PNS) on alveolar epithelial to mesenchymal transition (EMT) and extracellular matrix degradation were observed in a type of human alveolar epithelial cell, A549 cells, stimulated by TGF-beta1. Firstly, MTT method was applied to evaluation of cellular proliferation and found that PNS from 12.5 mg x L(-1) to 200 mg x L(-1) dosage could not inhibit significantly cellular proliferation. Then, cells were divided into five groups, normal group, TGF-beta1 group, TGF-beta1 + 50 mg x L(-1) PNS group, TGF-beta1 + 100 mg x L(-1) PNS group and TGF-beta1 + 200 mg x L(-1) PNS group. Normal cells were not stimulatec by TGF-beta1; TGF-beta1 cells were only stimulated by TGF-beta1 and the other cells were stimulated by TGF-beta1 with different doses of PNS, respectively. After stimulation, cells and supernatants were collected for assays. Cellular roundness was applied to quantitative evaluation of morphological change. Immunocytochemistry was applied to examine E-cadherion, a-SMA and FN proteins expression in the cells. Enzyme linked-immunosorbent assay was applied to MMP-9 and TIMP-1 levels. The results showed that EMT of A549 cells was induced by TGF-beta1, showing significant change of roundness, E-cadherion, alpha-SMA and FN (P < 0.05, P < 0.01). Compared to TGF-beta1, PNS significantly inhibited the changes of roundness (P < 0.05), FN and alpha-SMA (P < 0.05, P < 0.01) and not significantly inhibited the change of E-cadherion. Furthermore, MMP-9 levels were significantly increased by TGFbeta1 stimulation (P < 0.05), without significant change of TIMP-1. Compared with TGF-beta1, PNS could significantly increase MMP-9 level (P < 0.05) and decrease TIMP-1 levels (P < 0.05, P < 0.01). In conclusion, PNS could inhibit alveolar epithelial cell EMT induced by TGF-beta1, with increase of extracellular matrix degradation ability, which showed anti-fibrosis of lung ability.

Panax Notoginseng Saponins Ameliorates Coxsackievirus B3-Induced Myocarditis by Activating the Cystathionine-γ-Lyase/Hydrogen Sulfide Pathway.

This study is to determine the therapeutic effects of Panax notoginseng saponins (PNSs) on coxsackievirus B3 (CVB3)-induced myocarditis, and whether cystathionine-γ-lyase (CSE)/hydrogen sulfide (H2S) pathway is involved. Mouse model of myocarditis was induced by CVB3 infection, and the mice were subjected to vehicle (saline) or drug treatments (sodium bisulfide (NaHS), propargylglycine (PAG), or PNSs). The results showed that there were inflammatory cell infiltrations, interstitial edemas, and elevated inflammatory cytokines, in CVB3-induced myocarditis. PAG administration increased, whereas NaHS treatment decreased the severity of the myocarditis. PNS treatment dramatically alleviated these myocardial injuries and decreased the viral messenger RNA (mRNA) expression by the enhanced expression of CSE/H2S pathway. Moreover, the therapeutic effects of PNSs on myocarditis were stronger than those of NaHS. Finally, the effect of PNSs on CSE/H2S pathway and cardiac cell protection were verified in cultured cardiac cells. PNSs may be a promising medication for viral myocarditis therapy.

Effect of panax notoginseng saponins on pulmonary artery pathology of pulmonary hypertension rats

Objective To observe the effect of panax notoginseng saponins on pulmonary artery pathology in chronic hypoxic pulmonary hypertensionp (HPH) rats models, discuss the role and possible mechanisms of panax notoginseng saponins in prevention of chronic hypoxic pulmonary hypertension. Methods Forty male Sprague-Dawley (SD) rats were randomly divided into four groups (n=10). Group C: control group; Group H: rats were treated with hypoxia only; Group HC: rats were treated with hypoxia and captopril; and Group HP: rats were treated with hypoxia and panax notoginseng saponins. To observe the effect of panax notoginseng saponins prophylactic treatment in chronic hypoxic pulmonary hypertension rats, after the establishment of the model of hypoxic rat animal pulmonary hypertension models, transthoracic direct pulmonary artery intubation was measured in rat pulmonary arterial systolic pressure and mean pulmonary artery pressure, at the end of separation and cut for pulmonary artery to observe the pathological changes of pulmonary artery, results were recorded and statistically analyzed. Results ⑴Transthoracic direct pulmonary artery intubation was measured in rat pulmonary arterial systolic pressure and mean pulmonary artery pressure: pulmonary artery systolic pressure (PASP) and mean pulmonary arterial pressure (MPAP) were significantly higher in Group H than in Group C (P<0.05), Group HP was no significant difference relative to Group C. ⑵Pathological section shew that the primary pathological change of group H is vascular intimal hyperplasia and the proliferation of smooth muscle cells, medial hypertrophy, extracellular matrix increased, thickening of the vessel wall and the vascular stenos. Conclusions Panax notoginseng saponins inhibit the formation of chronic hypoxic pulmonary hypertension and pulmonary vascular remodeling in rats, and have the effect of prevention and treatment of pulmonary hypertension. Key words: SANCHINOSIDE/PD; Hypertension, pulmonary/DT/PA; Pulmonary artery/PA; Anoxia

The effects of Panax notoginseng saponins on the cytokines and peritoneal function in rats with peritoneal fibrosis

Background: Due to the long-term and chronic exposure to the peritoneal dialysis fluid, patients could develop peritoneal fibrosis and ultrafiltration failure which compromises treatment efficacy and outcome, and fibrosis is the major cause of peritoneal dialysis (PD) withdraw among patients. Methods: Twenty-one male WISTAR rats were randomly assigned to three groups, namely saline group, standard peritoneal dialysis fluid (PDF) group, and panax notoginseng saponins (PNS) group. Peritoneal fibrosis was induced by daily injection of PDF for 4 weeks. After execution, multiple histological techniques including HE and Masson's trichrome staining and transmission electron microscopy (TEM) were applied to observe the pathological changes and concentrations of multiple cytokines may involve in the process of fibrosis were determined by enzyme-linked immune sorbent assay (ELISA). Biochemistry parameters were determined by automated chemistry analyzer. Results: PNS can significantly inhibit the expression of transforming growth factor beta (TGF-β1), connective tissue growth factor (CTGF), and monocyte chemoattractant protein (MCP-1) in the peritoneum of rats. Furthermore, pathological damages, including extracellular matrix deposition, vascularization, and fibroblast, were ameliorated in PNS group when being compared with standard PDF group. Peritoneal functions were improved by regular PNS treatment with significantly elevated ultrafiltration. Conclusion: PNS is capable of improving peritoneal function in subjects with PDF exposure and can possibly applied in patients with PD after further verification.

Protective effect of panax notoginseng saponins on acute ethanol-induced liver injury is associated with ameliorating hepatic lipid accumulation and reducing ethanol-mediated oxidative stress.

The aim of present study was to evaluate the effects of Panax notoginseng saponins (PNS) against acute ethanol-induced liver injury and further to elucidate its probable mechanisms. Mice were treated with PNS (100 or 300 mg/kg) once daily for seven consecutive days priors to ethanol gavage (4.7 g/kg) every 12 h for a total of three doses. Acute alcohol gavage dramatically significantly increased serum activities of alanine aminotransferase (ALT) (23.4 ± 5.0 IU/L vs 11.7 ± 4.1 IU/L) and aspartate aminotransferase (AST) (52.6 ± 14.9 IU/L vs 31.1 ± 12.9 IU/L), and hepatic triglyceride level (4.04 ± 0.64 mg/g vs 1.92 ± 0.34 mg/g), these elevations were significantly diminished by pretreatment with PNS at dose of 100 mg/kg or 300 mg/kg. Alcohol exposure markedly induced the lipolysis of white adipose tissue (WAT), up-regulated protein expression of the phosphorylated hormone-sensitive lipase (p-HSL, p < 0.01), and total HSL (p < 0.01), and enhanced fatty acid uptake capacity in liver as indicated by increasing hepatic CD36 expression (p < 0.01), these effects were attenuated by PNS treatment. Additionally, PNS suppressed the elevation of reactive oxygen species (ROS) production and malondialdehyde (MDA) content, reduced TNF-α and IL-6 levels, restored glutathione (GSH) level, enhanced the superoxide dismutase (SOD) activity in liver, and abrogated cytochrome P450 2E1 (CYP2E1) induction. These data demonstrated that pretreatment with PNS protected against acute ethanol-induced liver injury, possibly through ameliorating hepatic lipid accumulation and reducing CYP2E1-mediated oxidative stress. Our findings also suggested that PNS may be potential to be developed as an effective agent for acute ethanol-induced liver injury.

Panax Notoginseng Saponins Restrains Ischemiareperfusion-induced Rat Mesenteric Microcirculatory Disturbance

Objective: To investigate the effect of Panax notoginseng saponins (PNS) on ischemia reperfusion (I/R) induced rat mesenteric microcirculatory dysfunctions. Methods: Male Wistar rats weighting 200–250 g were subjected to 10 min ligation of the superior mesenteric artery and vein, followed by 60 min reperfusion. PNS (5 mg/kg/hr) was continuously administrated starting from 10 min before ischemia or 10 min after reperfusion until 60 min after reperfusion via left jugular vein. Leukocytes adhesion, mast cell degranulation, endothelial peroxidation, and albumin leakage of rat mesenteric venules were observed. Serum myeloperoxidase (MPO) level, intercellular adhesion molecule-1 (ICAM-1) expression and Src phosphorylation were examined. Results: PNS ameliorated leukocyte adhesion and mast cell degranulation, while with no obvious effects on endothelial peroxidation and albumin leakage. In addition, PNS inhibited serum MPO increase, intestinal ICAM-1 expression and Src phosphorylation induced by I/R. Conclusions: PNS ameliorated I/R-induced leukocyte adhesion and mast cell degranulation, the former is related to its inhibition of Src phosphorylation and ICAM-1 expression. Abbreviations: DHR, Dihydrorhodamine-123; FITC, Fluorescein isothiocyanate; ICAM-1, intercellular adhesion molecule-1; I/R, ischemia-reperfusion; MPO, myeloperoxidase; NF-κB, nuclear factor-kappa B; PN, Panax notoginseng; PNS, Panax notoginseng saponins; p-Src, phosphor-Src; TNF-α, tumor necrosis factor.

Effect of PNS on Mobilizing Bone-marrow Mesenchymal Stem Cells in Rats

Objective: To investigate the effects of panax notoginseng saponins on mobilizing bone marrow mesenchymal stem cells after cerebral infarction so as to provide experimental basis for Huoxue Huayu Decoction (HXHYD) that is promoting the blood flow and removing blood stasis. Methods: Apart from the normal group, all of the remaining rats must survive the improved Zea-Longa middle cerebral artery occlusion (MCAO) modeling method; all standard rats were randomly divided into four groups. The first group designated as control group was administered with normal saline by gavage every day. The second, third and fourth groups designated as drug groups were administered respectively with Xuesaitong soft Capsule (ingredients dissolved in normal saline) in 20, 40 and 60 mg/ml body weight/day (low-dose group, mid-dose group and high-dose group). The treatment continued for 28 days. Each group was then divided into subgroups (each subgroup contains at least 8 rats) determined by time points (1st day 3rd day 7th day 14th day and 28th day). Changes of CD54, CD106, CD105, CD117 in blood and bone marrow of rats were detected by FCM. The SCF level at different time points were determined though ELISA methods. Results: The stem cell factor (SCF) level in peripheral blood and bone marrow showed a significant increase in the control group and the treated group. The SCF in peripheral blood and bone marrow increased on the 1st day and reached a peak on the 14th day, then decreased in the peripheral blood gradually. The SCF level in peripheral blood showed a better increase in both medium-dose and high-dose groups than that of model group (p 0.05) between the lowdose group and the control group at each time point. Conclusion: PNS can mobilize the BMSCs to improve the levels in the peripheral blood.

Early Steroid-Induced Osteonecrosis of Rabbit Femoral Head and Panax notoginseng Saponins: Mechanism and Protective Effects.

Background. This study was aimed at investigating the pathogenesis of oxidative stress in steroid-induced avascular necrosis of the femoral head (SANFH) and at exploring the mechanism and protective effects of Panax notoginseng saponins (PNS) on early SANFH. Methods. 80 adult New Zealand rabbits were randomly divided into control group, model group, and PNS group. In model group, equine serum was injected into auricular vein; then methylprednisolone was injected into gluteus. In PNS group, PNS was applied for 14 consecutive days before methylprednisolone management. At different time points, serum and femoral heads were prepared for T-AOC, SOD, GSH-PX, ·OH, and MDA determination. Two weeks after steroid management, all femoral heads were assessed with MRI and HE staining. Results. Typical early osteonecrosis symptoms were observed in model group. Our results showed that PNS could significantly ameliorate the decrease of T-AOC level, improve SOD and GSH-PX activity, suppress ·OH ability, and augment MDA level. Besides, PNS improved MRI and pathological changes of the femoral head, markedly reducing the incidence of osteonecrosis. Conclusion. Based on our research, we found oxidative stress played a positive role in the occurrence of SANFH where reactive oxygen species was the direct cause. PNS could protect rabbits against early steroid-induced osteonecrosis of femoral head by its antioxidative effect.

Effect of panax notoginseng saponins injection on the p38MAPK pathway in lung tissue in a rat model of hypoxic pulmonary hypertension.

To investigate the effect of panax notoginseng saponins (PNS) injection on pulmonary artery pressure and the expression of p38MAPK in lung tissue of rats subjected to chronic hypoxia. Thirty adult male Sprague Dawley rats were randomly divided into three groups (ten in each group): rats in control group were exposed to normoxic condition and the rats in hypoxia group and PNS group were subjected to 4-week hypoxia, and PNS injection (50 mg · kg(-1) · d(-1)) was administrated intraperitoneally at 30 min in the PNS group daily before the rats were kept in the hypoxic chamber, while rats in the other two groups received equal dose of normal saline instead. After chronic hypoxia, mean pulmonary artery pressure (mPAP) and mean carotid artery pressure (mCAP) were measured. The heart and lung tissues were harvested, and right ventricle (RV) and left ventricle plus ventricular septum (LV+S) were weighed to calculate the ratio of RV/(LV+S). The expression of p38MAPK mRNA was determined by reverse transcription-polymerase chain reaction, the quantity of phosphorylated p38MAPK (p-p38MAPK) in rat lung tissues and pulmonary arterioles was determined by Western blot and immunohistochemistry. Compared with the control group, mPAP and the ratio of RV/(LV+S) in the hypoxia group were increased, the expression of p-p38MAPK in pulmonary arterioles and p38MAPK mRNA in the lung were higher (P<0.05). The changes of these parameters in the hypoxia group were significantly attenuated by PNS treatment (P<0.05). PNS injection was shown to prevent hypoxic pulmonary hypertension at least partly by regulating p38MAPK pathway.

Effect of Panax notoginseng saponins on liver drug metablic enzyme activity, mrna and protein expressions in rats

To study the effect of Panax notoginseng saponins (PNS) on liver drug metabolic enzyme activity, mRNA and protein expressions in rats. Male Wistar rats were randomly divided into nine groups. After administration of the test drugs, their liver microsomes, liver total RNA and total protein were extracted to detect the regulating effect of PNS on liver drug metabolic enzyme activity-related subtype enzymatic activity, mRNA and protein expression by substrate probe, quantitative PCR and Western Blot technology. The result of this experiment was that PNS could significantly induce CYP1A2 and CYP2E1 enzyme activity, mRNA expression, CYP2E1 protein expression level. PNS significantly induced CYP3A mRNA expression, but with no significant effect in CYP3A enzyme activity level. PNS had no significant effect CYP1A1 and CYP2B mRNA expressions and enzyme activity levels. PNS had selective regulations on different P450 subtypes, and the major subtypes were CYP1A2 and CYP2E1. In clinical practice, particularly in the combination with CYP1A2 and CYP2E1 metabolism-related drugs, full consideration shall be given to the possible drug interactions in order to avoid potential toxic and side effects. Meanwhile, whether the induction effect of CYP2E1 gets involved in ginsenoside's effect incavenging free radicals deserves further studies.

Anti‑inflammatory effects of Panax notoginseng saponins ameliorate acute lung injury induced by oleic acid and lipopolysaccharide in rats.

This study investigated the effect of Panax notoginseng saponins (PNS) on acute lung injury (ALI) induced by oleic acid (OA) and lipopolysaccharide (LPS). A total of 28 Wistar rats were divided into four groups: sham; sham + PNS; OA‑LPS‑induced ALI and ALI + PNS. Lung tissue histology, lung wet‑to‑dry (W/D) weight ratio, extravascular lung water (EVLW) and epithelial sodium channel α (αENaC) mRNA and protein expression were examined. In addition, levels of inflammatory cytokines, including tumor necrosis factor α (TNF‑α), interleukin (IL)‑6 and IL‑10, as well as total leukocyte and neutrophil counts, were analyzed in rat bronchoalveolar lavage fluid (BALF) and serum. ALI + PNS rats were observed to exhibit significantly lower pulmonary parenchymal damage and EVLW compared with ALI rats. Furthermore, total leukocyte and neutrophil counts, and levels of inflammatory cytokines were significantly decreased following PNS administration in ALI rats. In addition, the decrease in αENaC mRNA and protein expression observed in the lung tissue of ALI rats was partially restored following PNS treatment. PNS treatment was demonstrated to ameliorate OA‑LPS‑induced ALI, potentially through restoration of αENaC mRNA and protein expression and through PNS‑induced anti‑inflammatory effects.

Antioxidative effects of Panax notoginseng saponins in brain cells

Oxidative stress resulting from accumulation of reactive oxygen species (ROS) is involved in cell death associated with neurological disorders such as stroke, Alzheimer's disease and traumatic brain injury. Antioxidant compounds that improve endogenous antioxidant defenses have been proposed for neural protection. The purpose of this study was to investigate the potential protective effects of total saponin in leaves of Panax notoginseng (LPNS) on oxidative stress and cell death in brain cells in vitro. Lactate dehydrogenase (LDH) assay indicated that LPNS (5μg/ml) reduced H2O2-induced cell death in primary rat cortical astrocytes (23±8% reduction in LDH release vs. control). Similar protection was found in oxygen and glucose deprivation/reoxygenation induced SH-SY5Y (a human neuroblastoma cell line) cell damage (78±7% reduction vs. control). The protective effects of LPNS in astrocytes were associated with attenuation of reactive oxygen species (ROS) accumulation. These effects involved activation of Nrf2 (nuclear translocation) and upregulation of downstream antioxidant systems including heme oxygenase-1 (HO-1) and glutathione S-transferase pi 1 (GSTP1). These results demonstrate for the first time that LPNS has antioxidative effects which may be neuroprotective in neurological disorders.

Effect of panax notoginseng saponins on renal cortical tubule cell Bax in early stage after renal trauma in rats

Objective To measure the effect of panax notoginseng saponins (PNS) on renal cortical tubule cell apoptosis and apoptosis-related genes in early stage after renal trauma and to investigate the protective mechanism of PNS for renal trauma.Methods Seventy-eight Wistar rats were divided into trauma group (n =36),trauma + treatment group (treatment group,n =36),normal control group (control group,n =6) according to the random number table.In treatment group,rats received intraperitoneal administration of PNS (70 mg/kg).Instead,substitute of an equal dose of isotonic saline was used for the rats in trauma and normal control groups.Trauma and treatment groups were subdivided at 1,6,12,24,36 and 48 hours posttrauma,with 6 rats per group.The kidney specimens were extracted at each time point to detect Bax expression in the cortex with immunohistochemistry and in situ hybridization histochemistry.Moreover,the positive expression of Bax was compared among groups and its variation regularity with time were detected.Results In trauma group,mRNA transcription of pro-apoptosis gene Bax increased at 12 hours in the superficial cortex,but increased at 1 hour in deep cortex; protein expression of pro-apoptosis factor Bax showed no apparent reduction within 36 hours in the superficial cortex,but evident decrease within 12 hours in the deep cortex.In treatment group,mRNA transcription of pro-apoptosis gene Bax decreased immediately after treatment in the renal cortex and lasted until 48 h; protein expression of pro-apoptosis factor Bax showed unidirectional reduction until 48 h in the renal cortex.Conclusion PNS inhibits cell apoptosis by down-regulating the mRNA and protein expression of Bax. Key words: Wounds and injuries; Kidney; Apoptosis; Kidney cortex necrosis

Effects of Panax notoginseng saponin on α, β, and γ secretase involved in Aβ deposition in SAMP8 mice

Our previous studies have shown that Panax notoginseng saponins (PNS) play a protective role in learning dysfunction of Alzheimer's disease, inhibit the deposition of Aβ1-40 and Aβ1-42, and reduce the content of App in the brain of SAMP8. In this study, we aimed to investigate the effects of PNS on α, β, and γ secretase involved in Aβ generation in SAMP8 mice. The results showed that PNS increased α-secretase activity perhaps by enhancing the level of ADAM9 expression, which itself was achieved by upregulating the expression of the ADAM9 gene. In addition, PNS significantly decreased BACE1 protein level by downregulating the level of BACE1 gene expression and consequently precluded the activity of β secretase. However, PNS treatment did not modify γ-secretase activity. Together, our study shows that PNS modulates the levels of protein and gene expressions involved with α and β secretase, thereby increasing α-secretase activity and reducing β-secretase activity, which may be one of the mechanisms of PNS precluding Aβ generation. Accordingly, PNS may be a promising agent for Alzheimer's disease.

Neuroprotective effect of panax notoginseng saponins and its main components

Stroke is the third leading cause of death and the first cause of adult disability in industrial countries [1]. It is charicaterized by hemiplegia, hemianopsia, aphasia, mouth askew and sever sequelae. It is considered that an ischemic disease without any specific treatment method and few effective drugs such as tPA (human tissue-type plasminogen activator) and Edarovone with specific therapeutic window will cause a lot of disadvantages if being used inaccurate. Root of Panax notoginseng (PN) which is one of traditional Chinese medicines (TCMs), was first found in “Shennong’s Classic of Materia Medica” around 200 AD. Panax notogineng saponins(PNS) is a multi-components mixture containing ginseng and saponins as the most important bioactive components which are commonly used in clinical treatment. Also, ginseng and saponins form the main components of many herbal medicines in the market, e.g., Xueshuantong injection [2], Xuesaitong injection [3], Xuesaitong soft capsule [4] and so on. The main monomers of Panax notoginseng saponins (PNS) are Ginsenoside-Rb1, Gensenoside-Rg1, Gensenoside-Re, Gensenoside-Rd and Panax notoginseng saponins-R1 [5]. In this review, we found some important points as well as shortcomings that require special consideration. We therefore highlighted the advances in neuro-protection of PNS and its main monomers in the area of experimental research.