Protective effects of sodium humate and its zinc and selenium chelate on the oxidative stress, inflammatory, and intestinal barrier damage of Salmonella Typhimurium-challenged broiler chickens.

The objective of this study was to investigate the protective effects and mechanisms of dietary administration of sodium humate (HNa) and its zinc and selenium chelate (Zn/Se-HNa) in mitigating Salmonella Typhimurium (S. Typhi) induced intestinal injury in broiler chickens. Following the gavage of 109 CFU S. Typhi to 240 broilers from 21-d to 23-d aged, various growth performance parameters such as body weight (BW), average daily gain (ADG), average daily feed intake (ADFI), and feed ratio (FCR) were measured before and after infection. Intestinal morphology was assessed to determine the villus height, crypt depth, and chorionic cryptologic ratio. To evaluate intestinal barrier integrity, levels of serum diamine oxidase (DAO), D-lactic acid, tight junction proteins, and the related genes were measured in each group of broilers. An analysis was conducted on inflammatory-related cytokines, oxidase activity, and Nuclear Factor Kappa B (NF-κB) and Nuclear factor erythroid2-related factor 2 (Nrf2) pathway-related proteins and mRNA expression. The results revealed a significant decrease in BW, ADG, and FCR in S. typhi-infected broilers. HNa tended to increase FCR (P = 0.056) while the supplementation of Zn/Se-HNa significantly restored BW and ADG (P < 0.05). HNa and Zn/Se-HNa exhibit favorable and comparable effects in enhancing the levels of serum DAO, D-lactate, and mRNA and protein expression of jejunum and ileal tight junction. In comparison to HNa, Zn/Se-HNa demonstrates a greater reduction in S. Typhi shedding in feces, as well as superior efficacy in enhancing the intestinal morphology, increasing serum catalase (CAT) activity, inhibiting pro-inflammatory cytokines, and suppressing the activation of the NF-κB pathway. Collectively, Zn/Se-HNa was a more effective treatment than HNa to alleviate adverse impact of S. Typhi infection in broiler chickens.

Preparation, characterization, bacteriostatic efficacy, and mechanism of zinc/selenium-loaded sodium humate.

In recent years, metal-based complexes including selenium (Se) and zinc (Zn)-containing compounds have been widely explored for their therapeutic properties due to their roles in biological processes and modulation of diverse molecular targets. Humic acid, as a metal complexing agent, is also widely used in biomedical field. In this work, three kinds of modified sodium humate (HNa), including Zn-HNA, Se-HNa, and Zn/Se-HNa, were prepared by ion exchange reaction method. The modified HNa was characterized by X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), and elemental mapping. The bacteriostatic activity and mechanism of modified HNa against gram-positive and gram-negative bacteria were investigated by testing bacterial inhibition zone, minimum inhibitory concentration, and capacity to destroy integrity of the bacterial membrane, promoting ROS generation level and prevention of biofilms. FTIR results showed that HNa could combine with zinc ions and selenite ions. The main XRD peaks did not change significantly. In the modified HNa, the particle shape was irregular. Compared to HNa, Zn-HNA, and Se-HNa, Zn/Se-HNa showed the strongest bacteriostatic activity. Zn/Se-HNa exhibited high bacteriostatic activity against gram-negative bacteria (Escherichia coli, Salmonella typhimurium, Klebsiella pneumoniae) and gram-positive bacteria (Staphylococcus aureus), but showed weak antibacterial activity against another gram-positive bacteria, Bacillus subtilis. The bacteriostasis was achieved by altering the permeability of bacterial cell membranes, generating ROS, and preventing the formation of biofilms. In conclusion, Zn/Se-HNa has high bacteriostatic activity, making it a suitable alternative to antibiotics in fields like the treatment of trauma infections and animal husbandry. KEY POINTS: • Preparate and characterize zinc- and selenium-loaded sodium humate (Zn/Se-HNa). • The combination of Zn and Se enhanced the bacteriostatic activity of HNa. • Zn/Se-HNa alters the permeability of bacterial cell membranes and promotes generation of ROS.

Pharmacokinetics and pharmacodynamics of enrofloxacin treatment of Escherichia coli in a murine thigh infection modeling.

BACKGROUND: Enrofloxacin is an antibacterial drug with broad-spectrum activity that is widely indicated for veterinary use. We aim to develop the clinical applications of Enrofloxacin against colibacillosis by using the neutropenic mice thigh infection model. RESULTS: The minimum inhibitory concentration (MIC) distribution of 67 isolated E. coli strains to ENR was calculated using CLSI guidelines. Whereas, the MIC50 value calculation was considered as the population PD parameter for ENR against E. coli strains. The MIC values of 15 E. coli strains were found to be nearest to the MIC50 i.e., 0.25 µg/mL. Of all the tested strains, the PK-PD and E. coli disease model was established via selected E. coli strain i.e., Heilong 15. We analyzed the PK characteristics of ENR and its metabolite ciprofloxacin (CIP) following a single subcutaneous (s.c.) injection of ENR (1.25, 2.5, 5, 10 mg/kg). The concentration-time profiling of ENR within the plasma specimens was determined by considering the non-compartmental analysis (NCA). The basic PK parameters of ENR for the peak drug concentration (Cmax) and the area under the concentration-time curve (AUC) values were found to be in the range of 0.27-1.97 µg/mL and 0.62-3.14 µg.h/mL, respectively. Multiple s.c. injection over 24 h (1.25, 2.5, 5, 10 mg/kg at various time points i.e., 6, 8, 12, and 24 h respectively) were administered to assess the targeted PD values. The Akaike Information Criterion (AIC) was used to choose PD models, and the model with the lowest AIC was chosen. The inhibitory Emax model was employed to calculate the related PK-PD parameters. The results of our study indicated that there was a strong correlation between the AUC/MIC and various antibacterial activities (R2 = 0.9928). The target values of dividing AUC/MIC by 24 h for bacteriostatic action were 1-log10 reduction, 2-log10 reduction, and 3-log10 reduction 0.325, 0.4375, 0.63, and 0.95 accordingly. CONCLUSION: The identified pharmacodynamics targets for various antibacterial effects will be crucial in enhancing ENR clinical applications and serving as a key step in reducing bacterial resistance.

Protective effects of ginsenoside Rg2 against memory impairment and neuronal death induced by Aß25-35 in rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Ginsenoside Rg2 is an important ingredient of Panax ginseng which often appears in ancient prescriptions for forgetfulness. Ginsenoside Rg2 exert neuroprotective effects and could be a new potential medicine to treat AD. In our previous study, we reported that ginsenoside Rg2 appears protect PC12 cells against Amyloid ß-fragment (25-35) (Aß25-35)-induced apoptosis via the PI3K/Akt pathway. However, there are no in vivo studies on the protective effects of ginsenoside Rg2 on Aß-induced neurotoxicity. AIM OF THE STUDY: The present study was performed to investigate the protective effects of ginsenoside Rg2 against Aß25-35-induced memory impairment, and its underlying mechanisms in rats. MATERIALS AND METHODS: An Alzheimer's Disease (AD) rat model was established by injecting the rats with Aß25-35 (1 µg/µl). Cognitive performance was evaluated by the Morris Water Maze test (MWM). The brain sections were processed and neuronal apoptosis in the hippocampus was evaluated by Hematoxylin and Eosin staining (H&E). To explore the anti-neuronal apoptosis mechanism of ginsenoside Rg2, we analyzed the protein expression of Bcl-2/Bax, caspase-3, and phospho-protein kinase B/protein kinase B (p-Akt/Akt) via western blot. RESULTS: A significant improvement in cognitive function was observed in administrated ginsenoside Rg2 AD rats. The histological injury in hippocampus CA1 induced by Aß25-35 was inhibited following administration of the ginsenoside Rg2. Ginsenoside Rg2 increase the Bcl-2/Bax ratio, attenuate the cleavage of caspase-3, and enhance the phosphorylation of Akt. CONCLUSIONS: These findings suggest that ginsenoside Rg2 could ameliorate Aß25-35-induced cognitive dysfunction by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway.

Effect of early activity combined with early nutrition on acquired weakness in ICU patients.

INTRODUCTION: Intensive care unit-acquired weakness (ICU-AW) occurs in 25% to 100% of critically ill patients, and is associated with prolonged mechanical ventilation, extended ICU stay, and total hospital stay, increased hospital costs, higher risk of death, impaired physical function, and decreased quality of life. However, there are not any current guidelines that mention management of ICU-AW. The present study will evaluate the effects of a combination of early nutrition and early exercise compared to those of either early exercise alone or the standard care for patients in ICUs. METHODS: This is a 3-arm, parallel, randomized controlled trial including an estimated 147 critically ill patients aged ≥18 years recruited from the ICUs of 2 hospitals in Heilongjiang, China. Patients will be prospectively randomized 1:1:1 to receive early mobilization, early nutrition combined with early mobilization, or standard care (minimal exercises, experience-based initiation and enrollment of nutrition support). Outcomes are assessed at ICU discharge after baseline. The primary outcome is occurrence of ICU-AW according to the Medical Research Council scale at the end of treatment. Muscle strength, organ failure, functional independence, self-care ability, time of ICU stay, duration of mechanical ventilation, and ICU mortality are secondary outcome measures. DISCUSSION: This trial has the potential to identify a novel strategy for preventing or managing ICU-AW. The findings may increase the clinical knowledge about nutrition and mobilization interventions for people with ICU-AW, and contribute to the formation of practice guidelines for managing this condition. TRIAL REGISTRATION NUMBER: ChiCTR2000033482.

Lower body mass indices and near-target early energy nutrition therapy may increase intensive care unit-associated infections: A retrospective study in Guangzhou, China.

BACKGROUND AND OBJECTIVES: The optimal energy intake for early nutrition therapy in critically ill patients is unknown, especially in Chinese patients with a lower BMI. This study investigated the relationship between energy intake and clinical outcomes in this patient population. METHODS AND STUDY DESIGN: A retrospective study was carried out at a tertiary hospital. Critically ill patients were recruited and divided into 3 tertiles according to the ratio of actual/target energy intake during the first week of hospitalization in the intensive care unit (ICU) (tertile I, <33.4%; tertile II, 33.4%-66.7%; and tertile III, >66.7%). 60-day mortality and other clinical outcomes were compared. To adjust for potentially confounding factors, multivariate and sensitivity analyses were performed exclusively in patients who stayed in the ICU for ≥7 days. RESULTS: A total of 325 patients with a mean BMI of 22.5±4.7 kg/m2 were recruited. 60-day mortality was similar between the 3 tertiles. In the unadjusted analysis, tertile III had a longer length of stay in the ICU and at the hospital, longer duration of mechanical ventilation, and higher rate of ICU-associated infections, but only the latter showed a significant difference between the 3 tertiles in the multivariate and sensitivity analyses. Logistic regression analysis showed that energy groups was an independent risk factor for ICU-associated infections. CONCLUSIONS: Energy intake in early nutrition therapy influences risk of ICU-associated infections in Chinese critically ill patients with lower BMI. Furthermore, patients with near-target energy intake have more frequent ICU-associated infections.

Dihydromethysticin, a natural molecule from Kava, suppresses the growth of colorectal cancer via the NLRC3/PI3K pathway.

Dihydromethysticin (DHM), a natural compound derived from Kava, has been reported to be effective against mental disorders and some malignant tumors. However, little is known about the inhibitory effect of DHM on colorectal cancer (CRC). First, we examined the impact of DHM on human colon cancer cell lines, which demonstrated that DHM inhibits proliferation, migration, and invasion and promotes apoptosis and cell cycle arrest in colon cancer cells in vitro. Using small hairpin RNA, we inhibited nucleotide-oligomerization domain-like receptor subfamily C3 (NLRC3)/phosphoinositide 3-kinase (PI3K) pathway to elucidate the partial signaling of DHM-mediated tumor suppression. Additionally, using an ectopic human CRC model, we verified whether DHM inhibits tumor growth and angiogenesis via the NLRC3/PI3K pathway in vivo. Overall, DHM showed an inhibitory effect on CRC by altering cell proliferation, migration, invasion, apoptosis, cell cycle, and angiogenesis, possibly via the NLRC3/PI3K pathway. Thus, DHM may be a promising candidate for CRC therapy.

Effect of organic acids production and bacterial community on the possible mechanism of phosphorus solubilization during composting with enriched phosphate-solubilizing bacteria inoculation.

Enriched phosphate-solubilizing bacteria (PSB) agent were acquired by domesticated cultivation, and inoculated into kitchen waste composting in different stages. The effect of different treatments on organic acids production, tricalcium phosphate (TCP) solubilization and their relationship with bacterial community were investigated during composting. Our results pointed out that inoculation affected pH, total acidity and the production of oxalic, lactic, citric, succinic, acetic and formic acids. We also found a strong advantage in the solubilization of TCP and phosphorus (P) availability for PSB inoculation especially in the cooling stage. Redundancy analysis and structural equation models demonstrated inoculation by different methods changed the correlation of the bacterial community composition with P fractions as well as organic acids, and strengthened the cooperative function related to P transformation among species during composting. Finally, we proposed a possible mechanism of P solubilization with enriched PSB inoculation, which was induced by bacterial community and organic acids production.

The roles and mechanisms of homogalacturonan and rhamnogalacturonan I pectins on the inhibition of cell migration.

Our previous paper reported the structure of ginseng pectic polysaccharides related to the cell migration inhibitory effects, but the underlying mechanisms are poorly understood. In this manuscript, rhamnogalacturonan I (RGI)-rich pectins prepared from ginseng pectin were investigated for their effect on cell migration. The results indicated that the combination of homogalacturonan (HG) and RGI-rich pectins exerted stronger effects than either HG- or RGI-rich pectin alone. Further studies revealed that the effects of HG- and RGI-rich pectins were dependent on pretreatment, which caused alterations in cell morphologies such as cell size and shape, focal adhesion, and the organization of actin filaments, suggesting that HG and RGI pectins exert synergistic effects on cell migration, likely through different ways. Morphological data and quantitative cell adhesion and spreading assays showed that HG- and RGI-rich pectin treatment decreased cell adhesion and cell spreading on the substratum, suggesting that HG- and RGI-rich pectins may exert their effects on cell migration via decreasing cell adhesion and cell spreading. Additionally, we showed that L-929 cells expressed little galectin-3 (Gal-3) and that lactose, an inhibitor of Gal-3 did not block the activities of HG- and RGI-rich pectins, implicating that cell migration inhibited by pectin did not correlate to Gal-3.

Impact of phosphate-solubilizing bacteria inoculation methods on phosphorus transformation and long-term utilization in composting.

This study aimed to assess the effect of phosphate-solubilizing bacteria (PSB) application and inoculation methods on rock phosphate (RP) solubilization and bacterial community during composting. The results showed that PSB inoculation in different stages of composting, especially both in the beginning and cooling stages, not only improved the diversity and abundance of PSB and bacterial community, but also distinctly increased the content of potential available phosphorus. Redundancy analysis indicated that the combined inoculation of PSB in the initial stage with higher inoculation amount and in the cooling stage with lower inoculation amount was the best way to improve the inoculation effect and increase the solubilization and utilization of RP during composting. Besides, we suggested three methods to improve phosphorus transformation and long-term utilization efficiency in composts based on biological fixation of phosphates by humic substance and phosphate-accumulating organisms.

Pectic Bee Pollen Polysaccharide from Rosa rugosa Alleviates Diet-Induced Hepatic Steatosis and Insulin Resistance via Induction of AMPK/mTOR-Mediated Autophagy.

Despite it is used as a nutraceutical against diabetes and obesity, the mechanism of action of bee pollen is still unclear. Pectic bee pollen polysaccharide (RBPP-P) was isolated from Rosa rugosa, and its structure was characterized by 13C-NMR and Fourier transform-infrared spectroscopy (FT-IR). Using high glucose and fatty acids-treated HepG2 cells and high fat diet (HFD)-induced obesity mice, we detected its effect on insulin function and lipid metabolism based on autophagy. RBPP-P contained arabinogalactan, rhamnogalacturonan I, and homogalacturonan domains. In vivo studies demonstrated that RBPP-P markedly ameliorated insulin resistance, glucose intolerance, and liver steatosis in obese mice. The suppressive effects of RBPP-P on liver steatosis and triglyceride content were mediated by increased autophagy and lipase expression in liver. In AMPK knockdown cells (prkaa 1/2-/- MEF) and HFD-fed mice tissues (liver, gonadal white adipose, and inguinal white adipose), RBPP-P enhanced autophagy in AMPK/mTOR-dependent way in liver, but not in adipose tissue. These findings demonstrated that bee pollen polysaccharide alleviated liver steatosis and insulin resistance by promoting autophagy via an AMPK/mTOR-mediated signaling pathway, suggesting that RBPP-P could be a novel therapeutic agent used for the treatment of obesity and diabetes.

Relationship Between the Comprehensive Nutritional Index and the EORTC QLQ-H&N35 in Nasopharyngeal Carcinoma Patients Treated with Intensity-Modulated Radiation Therapy.

This study aimed to explore the relationship between the comprehensive nutritional index (CNI) and quality of life in nasopharyngeal carcinoma (NPC) patients receiving intensity-modulated radiation therapy (IMRT). The nutritional index, which includes total lymphocyte count, hemoglobin and albumin levels, body mass index, and usual body weight percentage, was evaluated pre-treatment and post-treatment in patients who underwent IMRT. The quality of life of NPC patients was measured by the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Head and Neck Cancer Module (EORTC QLQ-H&N35) at four time points: pre-treatment, post-treatment, and 3 and 6 mo after IMRT. A comprehensive nutritional model was used to assess the correlation with QLQ-H&N35. The nutritional index decreased significantly post-treatment. The CNI was associated with immunotherapy; the International Union Against Cancer (UICC) stage; concurrent chemotherapy; speech problems, trouble with social contact, feeling ill and having dental problems at pre-treatment; sexuality at 3 mos post-treatment; and sensory problems and xerostomia at 6 mo post-treatment (P < 0.05). The nutritional status and QLQ-H&N35 scores in NPC patients decreased during IMRT. Our study provides an alternative measure of the CNI to improve the QLQ-H&N35 evaluation system for patients with NPC.

Identification of natural products with neuronal and metabolic benefits through autophagy induction.

Autophagy is a housekeeping lysosomal degradation pathway important for cellular survival, homeostasis and function. Various disease models have shown that upregulation of autophagy may be beneficial to combat disease pathogenesis. However, despite several recently reported small-molecule screens for synthetic autophagy inducers, natural chemicals of diverse structures and functions have not been included in the synthetic libraries, and characterization of their roles in autophagy has been lacking. To discover novel autophagy-regulating compounds and study their therapeutic mechanisms, we used analytic chemistry approaches to isolate natural phytochemicals from a reservoir of medicinal plants used in traditional remedies. From this pilot plant metabolite library, we identified several novel autophagy-inducing phytochemicals, including Rg2. Rg2 is a steroid glycoside chemical that activates autophagy in an AMPK-ULK1-dependent and MTOR-independent manner. Induction of autophagy by Rg2 enhances the clearance of protein aggregates in a cell-based model, improves cognitive behaviors in a mouse model of Alzheimer disease, and prevents high-fat diet-induced insulin resistance. Thus, we discovered a series of autophagy-inducing phytochemicals from medicinal plants, and found that one of the compounds Rg2 mediates metabolic and neurotrophic effects dependent on activation of the autophagy pathway. These findings may help explain how medicinal plants exert the therapeutic functions against metabolic diseases.

Anti-hyperglycemic and anti-oxidative activities of ginseng polysaccharides in STZ-induced diabetic mice.

Neutral (WGPN) and acidic (WGPA) polysaccharides were fractionated from ginseng polysaccharide. WGPN and WGPA decreased fasting blood glucose by different manners of administration. Intra-gastric administration of WGPA showed a marked hypoglycemic effect, which may be related to its anti-oxidative activity. The results indicated that WGPA may have anti-diabetic potential.

The effective mechanism of the polysaccharides from Panax ginseng on chronic fatigue syndrome.

Ginseng acidic polysaccharide WGPA isolated from the root of Panax ginseng C. A. Meyer was fractionated into WGPA-A and WGPA-N by anion-exchange chromatography. The antifatigue activity of ginseng acidic polysaccharide WGPA has been reported in our previous research. This present study was designed to identify its active component and elucidate the mechanism for preventing chronic fatigue syndrome (CFS). WGPA, WGPA-A and WGPA-N were orally administered to mice once daily for 15 days. The effects of these compounds on physiological biomarkers of oxidative stress and on the morphology of the mitochondria in striated skeletal muscle were assessed. The results of forced swimming test-induced indicated that WGPA and WGPA-A could lengthen the swimming time, while WGPA-N could not. In addition, malondialdehyde and lactate dehydrogenase levels in serum were enhanced; while those of superoxide dismutase and glutathione peroxidase were lowered. Interestingly, the structural degeneration of mitochondria were all ameliorated. These findings suggested that WGPA-A is the active component of WGPA, it might have potential therapeutic effects for CFS and the oxidative stress might be involved in the pathogenesis. Our results also provided essential data for a better understanding of the antifatigue effects of P. ginseng extracts.

Neuroprotective effects of ginseng pectin through the activation of ERK/MAPK and Akt survival signaling pathways.

In this study, we investigated the neuroprotective activities of ginseng pectin (GP) against hydrogen peroxide (H2O2)-induced neuronal toxicity in different neuronal cells. GP selectively attenuated H2O2-induced damage up to 26% in primary cortical neuron cells and human glioblastoma U87 cells. Following H2O2 exposure, DAPI staining and neuron-specific ß-tubulin antibody probing indicated that GP maintained cell integrity and decreased nuclei condensation. Data from western blot analysis revealed that pre-treatment with GP increased the phosphorylation of both the extracellular signal-regulated kinases 1 and 2 (ERK1/2) and Akt in cortical neuron cells. However, the phosphorylation of ERK1/2 was increased, but that of Akt was decreased in U87 cells. These results suggest that the protective effects of GP against H2O2-induced apoptosis may be due to the activation of the phosphorylation of ERK1/2 and Akt; however, the mechanisms involved differ depending on the cell line. This neuroprotective property indicates that GP could serve as a potential therapeutic agent for neurodegenerative diseases.

Further analysis of the structure and immunological activity of an RG-I type pectin from Panax ginseng.

In this paper, we further analysed the structure of a type I rhamnogalacturonan (RG-I) pectin (WGPA-2-RG) fractionated from ginseng polysaccharides. Methylation and periodate oxidation analyses showed that WGPA-2-RG has a backbone consisting of alternating rhamnose (Rha) and galacturonic acid (GalA) residues and side chains consisting of type II arabinogalactan (AG-II). Partial acidic hydrolysis for 6h completely removed arabinose (Ara), partial galactose (Gal), but little GalA and Rha. During partial hydrolysis, the molecular weight of WGPA-2-RG decreased smoothly, suggesting that the Ara and cleavable Gal residues exist on the surface of the molecule, while GalA and Rha residues exist in the core of the molecule. The bioactivity assay showed that the arabinogalactan side chains of WGPA-2-RG are essential structures for stimulating NO secretion and lymphocyte proliferation. However, removal of the Ara and Gal residues through hydrolysis did not appreciably affect the ability of WGPA-2-RG to enhance macrophage phagocytosis.

Comparative studies of the antiproliferative effects of ginseng polysaccharides on HT-29 human colon cancer cells.

Ginseng polysaccharide has anticancer activity. However, the structure-activity relationship and the activity mechanism are still unclear. Therefore, it is necessary to study the anticancer activity of structurally different ginseng polysaccharide fractions and their potential mechanisms. Ginseng polysaccharide fractions and their temperature-modified products were assayed for their effects on HT-29 cell proliferation by MTT assay, on cell cycle progression by flow cytometry, and on caspase-3 activation by western blot analysis. The HG-rich ginseng pectin inhibited cell proliferation and induced cell cycle arrest in the G2/M phase. The temperature-modified HG-rich pectin had dramatically increased antiproliferative effect and induced apoptosis accompanied by the activation of caspase-3. Starch-like glucan and arabinogalactan of ginseng exhibited no antiproliferative effects. Even after temperature modification, their inhibitory effects either remained unchanged or increased slightly. The HG-rich pectin exerts its antiproliferative effect via cell cycle arrest and the temperature modification markedly increased the antiproliferative effect.

In vivo antimalarial activities of glycoalkaloids isolated from Solanaceae plants.

CONTEXT: Malaria is one of the most common and serious protozoan tropical diseases. Multi-drug resistance remains pervasive, necessitating the continuous development of new antimalarial agents. OBJECTIVE: Many glycosides, such as triterpenoid saponins, were shown to have antimalarial activity against Plasmodium falciparum in vitro. This study was to elucidate the ability of five glycoalkaloids against Plasmodium yoelii and develop new antimalarial lead compounds. MATERIALS AND METHODS: Glycoalkaloids were isolated from three kinds of Solanaceae plants: chaconine and solanine were isolated from Solanum tuberosum L. sprouts, solamargine and solasonine from Solanum nigrum L. fruit, tomatine from Lycopersicon esculentum Mill. fruit. The five isolated glycoalkaloids were evaluated against Plasmodium yoelii 17XL in mice with 4-day parasitemia suppression test in different concentrations. RESULTS: Chaconine showed a dose-dependent suppression of malaria infection, ED50, 4.49 mg/kg; therapeutic index (TI), approximately 9. At a dose of 7.50 mg/kg, the parasitemia suppressions of chaconine, tomatine, solamargine, solasonine and solanine were 71.38, 65.25, 64.89, 57.47 and 41.30%, respectively. At 3.75 mg/kg, the parasitemia suppression of chaconine was 42.66%, but the derivative, chaconine-6-O-sulfate, appeared to show no antimalarial activity. Simultaneous administration of chaconine and solanine in 1:1 did not show any synergistic effects. DISCUSSION AND CONCLUSION: The results showed that the glycoalkaloids with chacotriose (chaconine and solamargine) were more active than those with solatriose (solanine and solasonine). Chaconine was the most active among the five glycoalkaloids. We propose that the activity is dependent upon non-specific carbohydrate interactions. The 6-OH of chaconine is important for antimalarial activity.

The inhibitory effect of ginseng pectin on L-929 cell migration.

We tested the effects of ginseng pectin prepared by enzymatic hydrolysis of ginseng polysaccharides on cell migration. Ginseng pectin impaired the migration of L-929 cells and reduced their migration speed by up to 50% of control in the presence or absence of serum, suggesting it worked on both serum-dependent and serum-independent migration pathways. Ginseng pectin impaired cell migration via decreased cell spreading. These findings represent a significant contribution towards understanding the bioactivities of ginseng polysaccharides and applying them to health food and medicine.