Panax Notoginseng Saponins Research Articles

<i>Astragalus membranaceus</i> and <i>Panax notoginseng</i> saponins improves intestinal l-arginine absorption and protects against intestinal disorder <i>in vivo</i>

Nutritional supplementation with L-arginine has been shown to promote cell growth and exercise performance, and is helpful to various disorders. Astragalus membranaceus and Panax notoginseng are traditional herbal medicines that display a wide range of beneficial activities. To understand their effects on L-arginine absorption in human intestinal cells, in vitro and in vivo experiments were performed using a standardized mixture of Astragalus membranaceus and Panax notoginseng saponins (APS). Our studies indicated that APS increased the expression of cationic amino acid transporter 1 (CAT1) and L-arginine transport in human Caco-2 cells. In addition, APS benefits TNBS-induced-colitis rats by increasing food intake, body weight, intestinal epithelial integrity, CAT1 gene expression, and blood L-arginine level. APS also reduces intestinal inflammation associated with increased myeloperoxidase activity in colitis rats. Further studies indicated that the plasma L-arginine level significantly increases in human subjects administered APS.

Living Chinese Herbal Scaffolds from Microfluidic Bioprinting for Wound Healing.

Biological scaffolds have been widely employed in wound healing applications, while their practical efficiency is compromised by insufficient oxygen delivery to the 3-dimensional constructs and inadequate nutrient supply for the long-term healing process. Here, we present an innovative living Chinese herbal scaffold to provide a sustainable oxygen and nutrient supply for promoting wound healing. Through a facile microfluidic bioprinting strategy, a traditional Chinese herbal medicine (Panax notoginseng saponins [PNS]) and a living autotrophic microorganism (microalgae Chlorella pyrenoidosa [MA]) were successfully encapsulated into the scaffolds. The encapsulated PNS could be gradually released from the scaffolds, which promoted cell adhesion, proliferation, migration, and tube formation invitro. In addition, benefiting from the photosynthetic oxygenation of the alive MA, the obtained scaffolds would produce sustainable oxygen under light illumination, exerting a protective effect against hypoxia-induced cell death. Based on these features, we have demonstrated through invivo experiments that these living Chinese herbal scaffolds could efficiently alleviate local hypoxia, enhance angiogenesis, and thereby accelerate wound closure in diabetic mice, indicating their great potential in wound healing and other tissue repair applications.

Retracted: Panax Notoginseng Saponin Rg1 Can Effectively Improve the Cognitive Function of 5 × FAD Mice.

[This retracts the article DOI: 10.1155/2022/5152761.].

Pharmacokinetics and Oral Bioavailability of Panax Notoginseng Saponins Administered to Rats Using a Validated UPLC–MS/MS Method

Panax notoginseng saponins (PNS) are the most important bioactive components of P. Notoginseng. In this paper, an evaluation of the pharmacokinetics and oral absolute bioavailability of PNS was carried out following intravenous and oral administration of PNS to Sprague-Dawley rats. The plasma concentration of 28 PNS was determined using a validated UPLC-MS/MS system. The results demonstrated that Rb1(32.8%), Rg1(41.4%), R1(9.4%), Re(4.5%), and Rd(3.5%) are the five main ingredients of PNS for administration. After oral administration, it was found that the area under the curve (AUC0-72h) for these five major saponins was significantly different. AUC0-72h of Rb1 and Rd accounted for about 60% of all PNS exposure, while AUC0-72h of Rg1 and R1 only accounted for 0.7%, and Re was undetectable in plasma. Also, PPD, PPT, and CK were detected as the major PNS metabolites in vivo. Furthermore, it was shown that the total oral bioavailability of PNS was only 1.2%.

Proteomic analysis revealed the pharmacological mechanism of Xueshuantong injection in preventing early acute myocardial infarction injury.

Background: Acute myocardial infarction (AMI) is a common and life-threatening cardiovascular disease. However, there is a lack of pathology and drug studies on AMI within 20min. Xueshuantong injection (XST) is mainly composed of Panax notoginseng saponins, which can dilate blood vessels and improve blood circulation, and is clinically used in the treatment of cardiovascular and cerebrovascular diseases. Purpose: The study aimed to investigate the protective mechanism of Xueshuantong injection against acute myocardial infarction within 20min in rats by proteomic methods and molecular docking. Method: The male Sprague-Dawley rat acute myocardial infarction model was established by LAD ligation, and Xueshuantong injection (38mg/kg) was injected into the caudal vein 15min before surgery. Cardiac function evaluation, morphological observation, label-free quantitative proteomics, Western blotting analysis, molecular docking, and affinity measurement were applied in this study. Results: In a span of 20min after acute myocardial infarction, the model group showed significant cardiac function impairment. Xueshuantong injection can significantly improve cardiac function and prevent pathological injury of myocardial tissue. A total of 117 vital differentially expressed proteins were identified by proteomic analysis, including 80 differentially expressed proteins (DEPs) in the sham group compared with model rats (Sham: model) and 43 DEPs in model rats compared with the Xueshuantong injection group (Model: XST). The treatment of Xueshuantong injection mainly involves "poly(A) RNA binding" and "cadherin binding involved in cell-cell adhesion." The differentially expressed levels of the pathways related to proteins Echdc2, Gcdh, Dlst, and Nampt, as well as 14-3-3 family proteins Ywhaz and Ywhab, could be quantitatively confirmed by WB. Molecular docking analysis and SPR analysis revealed that Ywhaz has a generally stable binding with five Xueshuantong injection components. Conclusion: Xueshuantong injection (XST) could protect rat myocardial function injury against AMI in 20min. Echdc2, Ywhaz, Gcdh, Ywhab, Nampt, and Dlst play an essential role in this protective effect. In particular, Ywhaz might be the core target of Xueshuantong injection when treating acute myocardial infarction in the early stage. This study promoted the understanding of the protective mechanism of Xueshuantong injection in 20min injury of acute myocardial infarction and contributed to the identification of possible targets of Xueshuantong injection.

Separation of Panax notoginseng saponins on modified rosin ester-bonded silica stationary phase and its mechanism

A column prepared using a unique three-membered phenanthrene skeleton of rosin has complementary selectivity to a C18 column for some separation tasks. In this study, propylene pimaric acid (16-hydroxyethyl acrylate-34-n-butyl) ester (BRB) and propylene pimaric acid (16-hydroxyethyl acrylate-34-dodecyl) ester (BRLA) were used as functional ligands to prepare two novel stationary phases, namely BRB@SiO2 and BRLA@SiO2, through a “thiol-ene” click chemistry reaction. The characterization results of Fourier transform infrared spectroscopy, thermogravimetric analysis, nitrogen adsorption-desorption measurements, and contact angle tests showed that the BRB@SiO2 and BRLA@SiO2 stationary phases were successfully prepared. In addition, the performance of the columns was evaluated using the Tanaka test and hydrophobic subtraction model, which showed that the stationary phases exhibited typical reversed-phase chromatography performance and good hydrophobicity, hydrophobic selectivity, and steric selectivity. The changes in the retention of Panax notoginseng saponins on a column under different chromatographic conditions (acetonitrile content, flow rate, and column temperature) were investigated. The separation effect of BRB@SiO2 and BRLA@SiO2 columns on P. notoginseng saponins was better than that of the C18 column and the BRLA@SiO2 column could replace the C18 column for the detection of P. notoginseng saponins.

Retraction Note: Effects of Panax notoginseng saponins on severe acute pancreatitis through the regulation of mTOR/Akt and caspase-3 signaling pathway by upregulating miR-181b expression in rats

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s12906-018-2118-8.

Panax notoginseng Alleviates Colitis via the Regulation of Gut Microbiota.

Gut microbiota are significantly associated with the occurrence and development of inflammatory bowel disease (IBD). Panax notoginseng saponins (PNS) could be used for colitis and to modulate gut microbiota. However, the mechanism behind the effects of PNS on anti-colitis that are pertinent to gut microbiota is largely unknown. This study aimed to evaluate the anti-colitis effects of PNS and explore the involved mechanism as it is related to gut microbiota. Results showed that PNS significantly alleviated dextran sulfate sodium (DSS)-induced colitis. Meanwhile, after PNS treatment, the tight junction proteins were enhanced and proinflammatory cytokines, such as TNF-[Formula: see text], IL-6, IL-1[Formula: see text], and IL-17, were decreased. Furthermore, Bacteroides spp. were significantly increased after modeling, while PNS reduced their abundance and significantly increased the amount of Akkermansia spp. in vivo. Importantly, Akkermansia spp. and Bacteroides spp. were correlated with the IBD disease indicators. Moreover, fecal microbiota transplantation (FMT) experiments confirmed that PNS-reshaped gut microbiota significantly alleviated DSS-induced colitis, while A. muciniphila significantly reduced the levels of the LPS-induced cellular inflammatory factors IL-1[Formula: see text] and TNF-[Formula: see text]. In conclusion, PNS alleviated colitis pertinent to the upregulation of Akkermania spp. and downregulation of Bacteroides spp. in the gut.

Panax notoginseng saponins alleviate damage to the intestinal barrier and regulate levels of intestinal microbes in a rat model of chronic kidney disease

Objectives Chronic kidney disease (CKD) is a long-term condition characterized by poor prognosis and a high mortality rate. Panax notoginseng saponins (PNS) are the main active ingredient of the traditional Chinese herb Panaxnotoginseng(Burk.)F.H.Chen, which has been widely reported to have various pharmacological effects. Here, we examined the effect of PNS on renal function and the modulation of intestinal flora and intestinal barrier in a rat model of adenine-induced CKD. Methods Adenine was used to establish a rat model of CKD, biochemical testing, histopathologic examination, ELISA, immunohistochemical assay, western blot assay, and fecal microbiota 16s rRNA analysis was used to test the effect of PNS on CKD rats. Results Adenine induced a significant decrease in glomerular filtration rate, an increase in urinary protein excretion rate, and pathological damage to renal tissue in CKD rats. TNF-α, MCP-1, IL-1β, IL-18, TMAO, and endotoxin levels were increased in the blood of the model rats. Application of PNS countered the effects of adenine, restoring the above parameters to the level observed in healthy rats. In addition, activation of the inflammatory proteins NF-κB (p65) and NLRP3 and the fibrosis-associated proteins α-SMA and smad3 were inhibited in the kidneys of CKD rats. Furthermore, PNS promoted the expression of the tight junction proteins Occludin and ZO-1, increased SIgA levels, strengthened intestinal immunity, reduced mechanical damage to the intestine, was reduced levels of DAO and D-LA. Our data suggest PNS may delay CKD by restoring gut microbiota, and through the subsequent generation of a microbial barrier and modulation of microbiota metabolites. Conclusions In conclusion, PNS may inhibit the development of inflammation and fibrosis in the kidney tissue through regulation of intestinal microorganisms and inhibition of the activation of pro-inflammatory and pro-fibrotic proteins in the kidney.

Panax notoginseng Saponins Attenuate Cerebral Ischemia-Reperfusion Injury via Mitophagy-Induced Inhibition of NLRP3 Inflammasome in Rats.

The mitophagy/NLRP3 inflammasome pathway is a promising therapeutic target for cerebral ischemia-reperfusion (I/R). Panax notoginseng (Burkill) F.H. Chen, one of the most valuable components of traditional Chinese medicine, and Panax notoginseng saponins (PNS), the main active ingredients of P. notoginseng, are patent medicines commonly used to treat cardio- and cerebrovascular diseases. However, their effects on the mitophagy and the NLRP3 inflammasome activation in I/R remain unclear. Therefore, in this study, we investigated how PNS might affect the mitophagy/NLRP3 inflammasome pathway in I/R. Cerebral I/R injury was induced by middle cerebral-artery occlusion, and expression levels of NLRP3 inflammasome signaling pathway-associated proteins were detected by western blot. We tested I/R injury using a neurological-deficit score, infarct volume, and hematoxylin and eosin staining, after which we detected both mitophagy- and NLRP3 inflammasome-related proteins in PNS-treated rats to determine whether PNS could attenuate I/R injury and the possible mechanisms involved. Our results showed that cerebral I/R could induce activation of the NLRP3 inflammasome, aggravating brain injury, whereas PNS effectively alleviated cerebral I/R injury in rats by inhibiting the NLRP3 inflammasome and promoting mitophagy via the PINK1/Parkin pathway. Moreover, mitophagy inhibited the NLRP3 inflammasome and mediated the anti-injury effects of PNS. In conclusion, PNS could promote mitophagy via the PINK1/Parkin pathway by inhibiting activation of the NLRP3 inflammasome, alleviating cerebral I/R injury in rats.

The therapeutic potential of natural products for treating pancreatic cancer.

Pancreatic cancer is one of the most malignant tumors of the digestive tract, with the poor prognosis and low 5-year survival rate less than 10%. Although surgical resection and chemotherapy as gemcitabine (first-line treatment) has been applied to the pancreatic cancer patients, the overall survival rates of pancreatic cancer are quite low due to drug resistance. Therefore, it is of urgent need to develop alternative strategies for its treatment. In this review, we summarized the major herbal drugs and metabolites, including curcumin, triptolide, Panax Notoginseng Saponins and their metabolites etc. These compounds with antioxidant, anti-angiogenic and anti-metastatic activities can inhibit the progression and metastasis of pancreatic cancer. Expecting to provide comprehensive information of potential natural products, our review provides valuable information and strategies for pancreatic cancer treatment.

Effects of panax notoginseng saponins on pulmonary vascular remodeling in rats with pulmonary hypertension and its mechanisms

Objective: To investigate the effects of panax notoginseng saponins (PNS) on pulmonary vascular remodeling and SIRT1/FOXO3a/p27 pathway in pulmonary arterial hypertension (PAH) rats. Methods: Male SD rats weighing 200~250g were randomly divided into control group, monocrotaline group (MCT) and monocrotaline + panax notoginseng saponins group (MCT+PNS), with 10 rats in each group. The rats in control group were injected intraperitoneally with normal saline 3 ml/kg on the first day, then injected intraperitoneally with normal saline 2.5 ml/kg every day. The rats in MCT group were injected intraperitoneally with MCT 60 mg/kg on the first day, followed by daily injection of normal saline 2.5 ml/kg. In MCT+PNS group, 60 mg/kg MCT was injected intraperitoneally on the first day, and 50 mg/kg PNS was injected intraperitoneally every day. The above models were fed conventionally for 4 weeks. After the modeling was completed, the mean pulmonary artery pressure (mPAP) and right ventricular systolic pressure (RVSP) of rats in each group were detected by right heart catheter method, weighed and calculated right ventricular hypertrophy index (RVHI), and the pulmonary vascular structure and morphological changes were observed by HE and Masson staining. The protein and gene expressions of SIRT1, FOXO3a, p27, PCNA and Caspase-3 were detected by qPCR and Western blot. Results: Compared with control group, mPAP, RVSP and RVHI in MCT group were increased significantly (P＜0.01), pulmonary vessels were thickened significantly and collagen fibers were increased, protein and gene expressions of SIRT1, FOXO3a, p27 and Caspase-3 were decreased (P＜0.05 or P＜0.01). The protein and gene expressions of PCNA were increased (P＜0.05). Compared with MCT group, the levels of mPAP, RVSP and RVHI in MCT+PNS group were decreased significantly (P＜0.05 or P＜0.01), pulmonary vascular thickening was alleviated and collagen fibers were reduced. The protein and gene expressions of SIRT1, FOXO3a, p27 and Caspase-3 were increased (P＜0.05 or P＜0.01), while the protein and gene expressions of PCNA were decreased (P＜0.05 or P＜0.01). Conclusion: Panax notoginseng saponins can relieve pulmonary vascular remodeling in rats with pulmonary hypertension by activating SIRT1/FOXO3a/p27 pathway.

Notoginsenoside R1 induces oxidative stress and modulates LPS induced immune microenvironment of nasopharyngeal carcinoma

BackgroundNasopharyngeal carcinoma (NPC) is a malignant tumor with high incidence. Notoginsenoside R1 (NGR1) is the main active compound of total Panax notoginseng saponin, and has multiple anti-tumor effects. This study aimed to investigate the effect and mechanism of NGR1 in NPC. MaterialsNPC cells were treated with different doses of NGR1. The NGR1 function in NPC was evaluated using Cell Counting Kit-8, Transwell, Western blot, flow cytometry, immunofluorescence assay, and quantitative real-time PCR. Meanwhile, the NGR1 mechanism in NPC was assessed by rescue experiments. Furthermore, the NGR1 function in vivo was determined by constructing an NPC xenotransplantation model, TUNEL, and immunohistochemistry assays. ResultsNGR1 repressed NPC cell growth and invasion but facilitated NPC cell apoptosis and oxidative stress. Also, NGR1 alleviated inflammation in NPC cells. Mechanistically, NGR1 restrained NPC cell growth and induced oxidative stress in NPC cells, while these effects were abolished after lipopolysaccharide (an activator of the TRAF6/NF-κB pathway) treatment, implying that NGR1 reduced NPC cell growth and induced oxidative stress in NPC cells by the inactivation of TRAF6/NF-κB axis. Moreover, in vivo studies further proved the palliative effect of NGR1 on NPC. ConclusionNGR1 inhibited NPC cell growth and induced oxidative stress in NPC cells by inactivating TRAF6/NF-κB axis.

Panax notoginseng saponins alleviates inflammation induced by microglial activation and protects against ischemic brain injury via inhibiting HIF-1α/PKM2/STAT3 signaling

Panax notoginseng saponins (PNS), the main active ingredient of herbal medicine Panax notoginseng, has been generally applied for the therapy of cardiovascular and cerebrovascular diseases, especially for stroke. It is believed that PNS has obvious anti-inflammatory effect, however, the roles of PNS on microglia after stroke have not been completely explored and the underlying mechanism of microglia-mediated inflammation remains to be clarified. In this study, cerebral ischemia injury was induced by photothrombotic (PT) stroke in mice. Two days after operation, PNS administration alleviated ischemic brain injury by increasing grip strength, relieving neurological deficits, improving local cerebral blood flow, and reducing pathological damage in the brain cortex and hippocampus. Moreover, microglial activation occurred in the acute stage after stroke and mediated inflammation, whereas PNS administration could inhibit microglial activation and inflammation. Meanwhile, we firstly demonstrated that PKM2 expression was upregulated in the nucleus of activated microglia after stroke, which could be inhibited after PNS administration. We hypothesized that suppression of nuclear PKM2 upregulation in microglia along with downregulation of HIF-1α/PKM2/STAT3 signaling could partially underlie the potential anti-inflammatory mechanism of PNS against ischemic brain injury. Our findings offer some new standpoints about PNS against microglia-mediated inflammation after stroke. Despite strengths, this study has limitation. PKM2 is not specifically expressed by microglia, but could be expressed by neurons, vascular endothelial cells, etc. Here we only explored the effect of PKM2 on activated microglia, and we would further investigate the impact of PKM2 expressed in other cells on stroke outcome in the future.

Analysis of the Renal Protection and Antioxidative Stress Effects of Panax notoginseng Saponins in Diabetic Nephropathy Mice.

Objective Diabetic nephropathy (DN), a diabetes-induced chronic complication, is the major trigger of end-stage renal disease. As the main active ingredient of Panax notoginseng (PNG), Panax notoginseng saponins (PNS) are crucial in treating renal diseases. This study is aimed at investigating the role played by PNS in renal protection and antioxidative stress (OS) in DN mice. Methods A DN mouse model was constructed, and then low, medium, and high doses of PNS were used to intervene the model group mice. Eight weeks after intervention, the 24 h urine protein (UPro) and urinary albumin (UAlb) were quantitatively examined, and the related blood biochemical indices were measured. HE and PAS staining were performed for pathological changes of renal tissue. ELISA and western blotting were carried out to quantify the levels of OS indexes and inflammatory factors (IFs) in mouse kidney tissues and the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), respectively. Results The weight of DN mice decreased first compared with control animals and then gradually increased after different doses of PNS treatment. Besides, DN mice presented elevated urine volume, UPro, and UAlb, all of which were reversed by PNS intervention. SOD activity and GSH content in renal tissues of the model group mice decreased markedly versus the control group, and MDA, CRP, IL-6, and TGF-β1 contents elevated statistically, while different doses of PNS effectively reduced the OS injury and IFs in mice. Compared with the model group, PNS dose-dependently increased Nrf2 and HO-1 levels in DN mice. Conclusions PNS is protective of HFF + STZ-induced DN mice against kidney tissue damage and can reduce the excretion of UPro and relieve the OS state of mice, possibly by activating Nrf2/HO-1 axis to play an antioxidant and anti-inflammatory role.

Biofilm Microenvironment-Mediated MoS2 Nanoplatform with Its Photothermal/Photodynamic Synergistic Antibacterial Molecular Mechanism and Wound Healing Study.

Drug-resistant bacterial infections pose a serious threat to human public health. Biofilm formation is one of the main factors contributing to the development of bacterial resistance, characterized by a hypoxic and microacidic microenvironment. Traditional antibiotic treatments have been ineffective against multidrug-resistant (MDR) bacteria. Novel monotherapies have had little success. On the basis of the photothermal effect, molybdenum disulfide (MoS2) nanoparticles were used to link quaternized polyethylenimine (QPEI), dihydroporphyrin e6 (Ce6), and Panax notoginseng saponins (PNS) in a zeolitic imidazolate framework-8 (ZIF-8). A multifunctional nanoplatform (MQCP@ZIF-8) was constructed with dual response to pH and near-infrared light (NIR), which resulted in synergistic photothermal and photodynamic antibacterial effects. The nanoplatform exhibited a photothermal conversion efficiency of 56%. It inhibited MDR Escherichia coli (E. coli) and MDR Staphylococcus aureus (S. aureus) by more than 95% and effectively promoted wound healing in mice infected with MDR S. aureus. The nanoplatform induced the death of MDR bacteria by promoting biofilm ablation, disrupting bacterial cell membranes and intracellular DNA, and interfering with intracellular material and energy metabolism. In this study, a multifunctional nanoplatform with good antibacterial effect was developed. The molecular mechanisms of MDR bacteria were also elucidated for possible clinical application.

Uncovering the effect and mechanism of Panax notoginseng saponins on metabolic syndrome by network pharmacology strategy

Ethnopharmacological relevanceMetabolic syndrome (MetS) is a cluster of disease centered on obesity, which is the result of stagnation of liver qi according to traditional Chinese medicine. Panax notoginseng is a traditional Chinese herbal medicine, entering liver and stomach meridians and dissipating blood stasis, in which panax notoginseng saponins (PNS) are the main active components. However, its effects and mechanism on metabolic syndrome has not been revealed yet. Aim of studyTo evaluate the anti-MetS effect of PNS, including body weight and adiposity, glucose metabolism and non-alcoholic fatty liver disease (NAFLD), as well as to explore the mechanism and signaling pathway of PNS on MetS effect. Materials and methodsHPLC was utilized to affirm the percentages of saponins in PNS. In vivo, normal C57BL/6J mice and high-fat diet (HFD)-induced MetS mice were used to evaluate anti-MetS effect of PNS. Body weight, food and water intake were recorded. NMR imager was used for NMR imaging and lipid-water analysis. Blood glucose detection, glucose and insulin tolerance test were performed to evaluate glucose metabolism. Biochemical indexes analysis and histopathological staining were used to evaluate the effect on NAFLD. The expressions of mRNA and proteins related to thermogenesis in adipose tissue were determined using real-time PCR and Western blot. In silico, network pharmacology was utilized to predict potential mechanism. In vitro, matured 3T3-L1 adipocyte was used as subject to confirm the signaling pathway by Western blot. ResultsWe determined the content of PNS component by HPLC. In vivo, PNS could improve metabolic syndrome with weight loss, reduction of adiposity, improvement of adipose distribution, correction of glucose metabolism disorder and attenuation of NAFLD. Mechanismly, PNS boosted energy exhaustion and dramatically enhanced thermogenesis in brown adipose tissue (BAT), induced white adipose tissue (WAT) browning. In silico, utilizing network pharmacology strategy, we identified 307 candidate targets which were enriched in MAPK signaling pathway specifically in liver tissue and adipocyte. In vitro validation confirmed ERK and p38MAPK mediated anti-MetS effects of PNS, not JNK signaling pathway. ConclusionPNS exerted protective effect on metabolic syndrome through MAPK-mediated adipose thermogenic activation, which may serve as a prospective therapeutic drug for metabolic syndrome.

Develop an ADR prediction system of Chinese herbal injections containing Panax notoginseng saponin: a nested case–control study using machine learning

ObjectiveThis study aimed to develop an adverse drug reactions (ADR) antecedent prediction system using machine learning algorithms to provide the reference for security usage of Chinese herbal injections containing Panax...

Feeding foliar nano-selenium biofortified panax notoginseng could reduce the occurrence of glycolipid metabolism disorder in mice caused by high-fat diets.

Nano-selenium (nano-Se) has been extensively explored as a biostimulant for improving the quality of grain crops. However, there are few reports about the effect on the medicinal components of Chinese herbal medicine cultured with nano-Se. Here, we sprayed nano-Se during the cultivation of Panax notoginseng (SePN), and measured the changes of medicinal components compared with conventional Panax notoginseng (PN). Furthermore, we identified a more pronounced effect of SePN on reducing obesity in animals compared with PN. By measuring antioxidant capacity, histopathology, gene expression related to glycolipid metabolism, and gut microbiota composition, we propose a potential mechanism for SePN to improve animal health. Compared with the control groups, foliar spraying of nano-Se increased saponins contents (Rb2, Rb3, Rc, F2, Rb2, and Rf) in the roots of Panax notoginseng, the content of Rb2 increased by 3.9 times particularly. Interestingly, animal studies indicated that taking selenium-rich Panax notoginseng (SePN) can further ameliorate liver antioxidation (SOD, MDA, and GSH) and enzyme activities involved in glycolipid metabolism (ATGL and PFK). It also relieved inflammation and regulated the expression of genes (MCAD, PPAR-α, and PCSK9) related to fatty acid oxidation. The abundance ratio of Firmicutes/Bacteroides and beneficial bacteria abundance (Bifidobacterium, Butyricimonas, and Parasutterella) in gut microbiota were improved relative to the control. In summary, the application of nano-Se on PN may effectively raise the content of Panax notoginseng saponins (PNS) and immensely lower the risk of metabolic disorders of glycolipids.

Pharmacological Effect of Panax notoginseng Saponins on Cerebral Ischemia in Animal Models.

Panax notoginseng saponins (PNS), bioactive compounds, are commonly used to treat ischemic heart and cerebral diseases in China and other Asian countries. Most previous studies of PNS have focused on the mechanisms underlying their treatment of ischemic cardiovascular diseases but not cerebral ischemic diseases. This study sought to explore the pharmacological mechanisms underlying the effectiveness of PNS in treating cerebral ischemic diseases. Different experimental cerebral ischemia models (including middle cerebral artery occlusion (MCAO) and the blockade of four arteries in rats, collagen-adrenaline-induced systemic intravascular thrombosis in mice, thrombosis of carotid artery-jugular vein blood flow in the bypass of rats, and hypoxia tolerance in mice) were used to investigate the mechanisms underlying the actions of PNS on cerebral ischemia. The results indicated that (1) PNS improved neurological function and reduced the cerebral ischemia infraction area in MCAO rats; (2) PNS improved motor coordination function in rats with complete cerebral ischemia (blockade of four arteries), decreased Ca2+ levels, and ameliorated energy metabolism in the brains of ischemia rats; (3) PNS reduced thrombosis in common carotid artery-jugular vein blood flow in the bypass of rats; (4) PNS provided significant promise in antistroke hemiplegia and hypoxia tolerance in mice. In conclusion, PNS showed antagonistic effects on ischemic stroke, and pharmacological mechanisms are likely to be associated with the reduction of cerebral pathological damage, thrombolysis, antihypoxia, and improvement in the intracellular Ca2+ overload and cerebral energy metabolism.