Objectives: Dendrobine (DDB) is one of the active ingredients in Dendrobium and has been reported to have significant neuroprotective properties. Nevertheless, the precise mechanisms underlying its action have not been fully clarified. The microglial imbalance of polarization is regarded as one of the key determinants in the etiology of neurodegenerative conditions, in the contribution of neuroinflammation. The recovery of M1/M2 balance and the inhibition of over-production of the pro-inflammatory effects have become major topics in modern studies of preventing and treating neurodegenerative diseases. Methods: Therefore, the present study aimed to explore the effects of DDB on the Lipopolysaccharide (LPS)-induced neuroinflammatory model in BV2 microglial cells and the potential molecular mechanisms of microglial M1/M2 polarization. Result: The results showed that DDB significantly suppressed Nitric Oxide (NO) release and ROS levels in LPS-induced BV2 cells. ELISA, qPCR, Western blot, and immunofluorescence results indicated that DDB reduced pro-inflammatory mediators Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6), and nterleukin-1 beta (IL-1β) and increased anti-inflammatory mediators Interleukin-10 (IL-10) and Arginase-1 (Arg-1). Consistently, it decreased M1-like markers Inducible Nitric Oxide Synthase (iNOS) and Cluster of Differentiation 16/32 (CD16/32) while increasing M2-like/repair-associated markers (CD206 and Arg-1), suggesting a shift toward a more anti-inflammatory microglial activation profile based on the assessed marker pane. Conclusions: These results suggested that DDB can suppress the production of inflammatory cytokines and modulate microglial polarization, which indicated that DDB can be used as an effective compound in the prevention of neuroinflammation-related disorders.
Cognitive impairment is a growing public health concern associated with aging, neurodegenerative diseases, and chronic stress. Polygonatum sibiricum Red. (P. sibiricum, Huang Jing), a traditional Chinese medicinal herb, is used to reinforce qi, strengthen the spleen, and nourish yin. Recent studies have suggested that P. sibiricum polysaccharides (PSP), its major bioactive constituents, exert neuroprotective effects through antioxidant and anti-inflammatory actions, modulation of the gut–brain axis, and improvement of synaptic plasticity. This review summarizes recent advances in the pharmacological activities of P. sibiricum and PSP related to cognitive improvement, highlights findings from behavioral, cellular, and molecular studies, and examines the clinical evidence supporting their therapeutic potential. Understanding the mechanism of action of P. sibiricum offers new insights into its potential development as a functional food or complementary therapeutic agent for cognitive decline.
Chronic sleep deprivation (CSD) disrupts redox homeostasis and enhances neuroinflammatory activation, contributing to progressive cognitive impairment. Propyl gallate (PG), a lipophilic ester of gallic acid with established antioxidant activity, has not been investigated in the context of prolonged sleep deprivation. The current study examined whether PG alleviates CSD-induced oxidative imbalance, inflammatory activation, and associated behavioral deficits. Male ICR mice were subjected to 14 days of CSD using a rolling-drum apparatus and received oral PG (50, 100, or 200 mg/kg) or Ginkgo biloba extract (GBE, 40 mg/kg). Behavioral outcomes were assessed through a battery of tests, including the open-field, novel-object recognition, step-through, and Morris water maze paradigms. Oxidative and inflammatory biomarkers were assessed in serum and hippocampus, and Western blotting quantified the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase 1 (NQO1), nuclear factor-κB (NF-κB), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX2). PG improved CSD-induced impairments in exploration, recognition memory, and spatial learning; restored antioxidant capacity; reduced lipid peroxidation; enhanced Nrf2-associated antioxidant signaling; and suppressed NF-κB-mediated inflammatory activation. These findings indicate that PG alleviates cognitive deficits induced by CSD through the modulation of redox homeostasis and neuroinflammatory responses, supporting its potential as an antioxidant derivative under chronic sleep-deprivation conditions.
Polygonatum kingianum (PK), a plant with established medicinal and nutritional applications, has shown potential neuroprotective activity in Alzheimer’s disease (AD). Nevertheless, the effects of its major bioactive fractions remain unclear. This study examined the neuroprotective effects of PK polysaccharides (PKPs) and saponins (PKSs) using an AlCl3-induced zebrafish model. Chemical analyses revealed that PKP was dominated by a low-molecular-weight fraction (1890 Da, 83.8%), whereas LC-MS analysis detected 13 tentatively identified steroidal saponins within PKS, including diosgenin. Furthermore, behavioral assessments demonstrated that both PKP and PKS improved locomotor and cognitive functions. PKP exhibited a stronger effect on the cholinergic system; its acetylcholinesterase (AChE) inhibitory activity at 60 μg/mL was comparable to that of donepezil under the experimental conditions. Histopathological analysis indicated that PKP showed a stronger effect in reducing neuronal apoptosis, resulting in a 68% reduction in the number of apoptotic cells. Conversely, PKS displayed a greater effect on amyloid pathology, reducing amyloid-beta (Aβ) aggregation by 62%. These findings suggest that PKP and PKS showed different neuroprotective profiles in the zebrafish model. Specifically, PKP was more closely associated with cholinergic regulation and neuronal survival, whereas PKS showed a stronger effect on Aβ aggregation. This study provides experimental support for the potential use of PK-derived fractions as food-derived bioactive components for alleviating AD-related pathological changes.
Chronic stress disrupts neuroendocrine regulation, neurotransmitter balance, and neuronal redox homeostasis, thereby contributing to the development of anxiety-related neuropathology. Arecoline, the predominant alkaloid of Areca catechu L., displays diverse neuropharmacological properties, yet its role in stress-induced emotional dysfunction has not been fully elucidated. This study examined the anxiolytic-like and neuroprotective effects of arecoline in mice exposed to chronic unpredictable mild stress (CUMS). Arecoline administration markedly improved behavioral outcomes, reflected by increased central exploration in the open-field test, prolonged time in the light compartment, and enhanced open-arm activity in the elevated plus maze. These behavioral benefits were accompanied by normalization of serum corticosterone levels, restoration of hippocampal neurotransmitters, reinforcement of antioxidant enzyme activities, and attenuation of pro-inflammatory cytokines. At the molecular level, arecoline elevated brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), cAMP response element-binding protein (CREB), N-methyl-D-aspartate receptor (NMDAR), and Ca2+/calmodulin-dependent protein kinase II (CaMKII), indicating enhanced synaptic plasticity, while concurrently diminishing oxidative and inflammatory stress. Collectively, the findings suggest that arecoline exerts multifaceted neuroprotective actions under chronic stress by coordinating neuroendocrine modulation, neurotransmitter homeostasis, antioxidant defenses, and synaptic plasticity. This study provides new mechanistic evidence supporting the potential relevance of arecoline as a functional neuroactive compound for managing stress-induced anxiety disorders.
The growing elderly population has heightened the demand for safe, nutritious foods for individuals with dysphagia. This study aimed to develop and characterize a novel alkali-induced gel system based on Dendrobium officinale polysaccharide (DOP) and hemp seed protein (HSP) for potential use in dysphagia-friendly formulations. A series of DOP-HSP gels (1.0-3.0 % DOP, w/v) were prepared, and their physicochemical properties, functional performance, and biocompatibility were systematically evaluated. The results demonstrated that increasing DOP content significantly enhanced the gel's water-holding capacity, mechanical strength, viscoelasticity, stability, and network uniformity. International Dysphagia Diet Standardization Initiative testing confirmed Level 5 for gels containing 1.0-2.5 % DOP, and Level 6 for 3.0 % DOP, meeting texture safety criteria for dysphagia care. Structural analysis revealed that DOP induced conformational changes in HSP, while mechanistic investigations indicated that disulfide bonding primarily contributed to the stabilization of the gel network. The 2.5 % DOP gel maximized antioxidant activity while reducing digestibility compared to pure HSP. Additionally, the excellent biocompatibility of the gels was confirmed by cytotoxicity assessment in Caco-2 cells. Collectively, these findings indicated that DOP content can effectively modulate gel texture and functionality, offering a viable approach for designing tailored food formulations for dysphagia.
Background: Gallic acid (GA) is a dietary polyphenol widely found in walnuts, tea leaves, and grapes, and it is recognized for its potent antioxidant and anti-inflammatory properties. Chronic sleep deprivation (CSD) is known to disrupt redox balance, promote neuroinflammation, and impair cognition, while effective nutritional strategies to mitigate these effects remain scarce. This study was designed to evaluate the protective potential of GA against CSD-induced cognitive deficits in mice and to elucidate the underlying mechanisms. Methods: Seventy-two male ICR mice were randomly allocated to six groups, including control, CSD model, Ginkgo biloba extract, and GA at three doses (50, 100, and 200 mg/kg). After 28 days of treatment, cognitive performance was assessed using the open field test (OFT), novel object recognition (NOR), step-through passive avoidance (ST), and Morris water maze (MWM). Redox status and inflammatory mediators were determined by ELISA, while the hippocampal expression of proteins related to antioxidant defense and NF-κB signaling was analyzed by Western blotting. Results: GA supplementation improved exploratory activity, recognition memory, and spatial learning in the CSD mice. Biochemical evaluation revealed that total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) activity were restored, while malondialdehyde (MDA) levels, an indicator of lipid peroxidation, were reduced. These changes were accompanied by decreased circulating concentrations of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). At the molecular level, GA enhanced the expression of Nrf2, HO-1, and NQO1, while inhibiting p-p65, iNOS, and COX2 in the hippocampus. Conclusions: These findings demonstrate that GA alleviates CSD-induced cognitive deficits through the activation of the Nrf2/HO-1 antioxidant pathway and inhibition of NF-κB–mediated inflammatory responses. Thus, GA may represent a promising nutraceutical candidate for maintaining cognitive health under chronic sleep loss.
Natural alkaloids derived from edible and medicinal plants have recently gained attention as bioactive molecules capable of modulating neuroinflammatory processes. Arecoline, the major alkaloid constituent of Areca catechu L. (betel nut), is well known for its cholinergic actions, yet its direct regulatory influence on microglial immune signaling has remained uncertain. In this study, murine BV2 microglial cells were employed to investigate whether arecoline could counteract lipopolysaccharide (LPS)-induced neuroinflammatory responses. Parameters including cell viability, nitric oxide (NO) production, cytokine secretion, and gene expression were assessed, and mechanistic analyses were focused on the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathways. Non-toxic doses of arecoline (10-40 μmol/L) markedly decreased NO accumulation and reduced the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Western blot analysis further showed that arecoline suppressed LPS-activated microglial signaling by down-regulating TLR4, inhibiting NF-κB p65 phosphorylation, and limiting PI3K/AKT activation. Collectively, these data reveal that arecoline exerts immunomodulatory and neuroprotective effects through dual signaling regulation in microglia and may serve as a useful pharmacological tool or structural reference for elucidating microglial inflammatory regulation and for guiding the exploration of safer bioactive compounds.
ETHNOPHARMACOLOGICAL RELEVANCE:Polygonatum sibiricum (PS) has a long-standing history of application in traditional Chinese medicine and various ethnic pharmacopeias to treat fatigue, aging-related weakness, memory decline, and metabolic disorders. It is believed to "tonify Qi and Yin," "nourish the kidney and spleen," and enhance vitality. Recent pharmacological studies have confirmed its antioxidant, neuroprotective, and anti-aging properties, suggesting its potential in improving cognitive impairment and neural damage, particularly under chronic stress or degenerative conditions. However, its mechanisms in memory-related disorders remain underexplored. AIM OF THE STUDY:This study aims to investigate the protective effects and underlying mechanisms of Polygonatum sibiricum polysaccharides (PSP) against neuronal damage induced by chronic stress. Specifically, the study evaluates the efficacy of PSP in ameliorating cognitive dysfunction, oxidative stress, neuroinflammation, and neurotransmitter imbalances in mouse models of chronic sleep disturbance (CSD) and chronic restraint stress (CRS). This research focuses on exploring the neuroprotective potential and underlying biological mechanisms of Polygonatum sibiricum polysaccharides (PSP) in response to neuronal injury caused by chronic stress. Specifically, the study evaluates the efficacy of PSP in ameliorating cognitive dysfunction, oxidative stress, neuroinflammation, and neurotransmitter imbalances in mouse models of CSD and CRS. MATERIALS AND METHODS:We developed chronic stress animal models by employing CSD and CRS. The ameliorative effects of PSP on stress-induced neuronal injury were assessed using a series of behavioral tests. Biochemical and histological assessments were conducted to investigate how PSP modulates oxidative stress, neuroinflammatory responses, and neurotransmitter homeostasis. RESULTS:PSP exert comprehensive neuroprotective effects in mice exposed to chronic stress, acting through multiple interconnected mechanisms. In behavioral assessments, PSP significantly improved cognitive performance in both CSD and CRS models. Mice treated with PSP showed shorter escape latency and more frequent platform crossings in the MWM, indicating enhanced spatial learning and memory. Similarly, improved outcomes in the NOR and OLR tests reflected better recognition and spatial memory, while performance gains in the OFT and ST suggested reduced anxiety-like behavior and improved associative learning. These behavioral enhancements were supported by marked reductions in hippocampal interleukin-6 (IL-6) and interleukin-1β (IL-1β) levels in CSD-treated mice, indicating potent anti-inflammatory activity. PSP also modulated neurotransmitter balance by increasing acetylcholine (ACh), critical for learning and memory, and decreasing γ-aminobutyric acid (GABA), which is often elevated under stress and associated with impaired cognition. PSP enhanced the antioxidant capacity in CRS mice, as evidenced by elevated activities of superoxide dismutase (SOD) and catalase (CAT) enzymes and a concurrent reduction in malondialdehyde (MDA) concentration, thereby protecting neurons from oxidative damage. Moreover, PSP reduced serum corticosterone (CORT) levels, reflecting its regulatory influence on the hypothalamic-pituitary-adrenal (HPA) axis and mitigating glucocorticoid-driven hippocampal impairment commonly associated with chronic stress. Collectively, these findings reveal that PSP not only alleviates behavioral deficits but also targets the underlying biochemical and hormonal disruptions caused by chronic stress, highlighting its therapeutic potential in preventing or treating stress-related cognitive disorders. CONCLUSION:This study demonstrates that PSP exert notable neuroprotective effects in chronic stress models by improving cognitive function, reducing oxidative stress and neuroinflammation, balancing neurotransmitter levels, and regulating HPA axis activity. These findings provide pharmacological support for the traditional use of PS in treating neurodegenerative and stress-related cognitive disorders.
An overproduction of reactive oxygen species (ROS) creates oxidative stress that disrupts neuronal activity and contributes to the pathogenesis of neurodegenerative diseases. Arecoline, the predominant alkaloid component of Areca catechu L., is known for multiple biological activities, yet its involvement in neuronal oxidative injury has not been fully clarified. This study investigated arecoline’s effect on hydrogen peroxide (H2O2)-induced toxicity in SH-SY5Y human neuroblastoma cells (SH-SY5Y). Arecoline pretreatment significantly improved cell viability and preserved plasma membrane integrity, accompanied by reduced lipid peroxidation and restoration of cellular antioxidant enzyme activities. Moreover, arecoline maintained mitochondrial membrane potential and suppressed apoptotic progression. At the molecular level, Arecoline stimulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) protein expression, concurrently diminishing Kelch-like ECH-associated protein 1 (Keap1) levels. In parallel, it altered the apoptosis profile by increasing B-cell lymphoma 2 (Bcl2) levels and decreasing Bcl-2-associated X protein (Bax) and total cysteine aspartate protease-3 (Caspase-3) protein expression. Collectively, the findings suggest that arecoline safeguards neurons against oxidative stress by simultaneously activating antioxidant defenses and restraining apoptosis. This study adds novel molecular evidence supporting the potential neuroprotective relevance of arecoline in oxidative stress-related neuropathology.
Dendrobium officinale (DO) is a perennial herb that has been utilized medicinal and edible purposes for thousands of years, often transforming into 'Fengdou' after drying. Despite its long-standing use, the specific phenolic components present during DO processing have remained elusive. This study established a method for the simultaneous and accurate quantification of 27 phenolic compounds during DO processing employing ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), with 8 reference-free components optimized through an online strategy. Furthermore, correlation analysis and molecular docking were conducted to further screened and validated 6 phenolics with alpha-glucosidase inhibitory activity, including vanillin, p-coumaric acid, 4-hydroxybenzaldehyde, resveratrol, coniferyl alcohol, and dihydropinosylvin. Notably, resveratrol exhibited the lowest binding energy at -7.7 kcal/mol among these compounds. These findings significantly contribute to the development of the deep-processing techniques for DO and the hypoglycaemic functional food industry by providing data that support the elucidation of medicinal substances in DO.
Polygonum sibiricum, with its medicinal and edibility dual properties, has been widely recognized and utilized throughout Chinese history. As a kind of its effective component, Polygonum sibiricum polysaccharides (PSP) have been reported to be a promising novel antidepressant agent. Meanwhile, the precise mechanisms underlying its action remain elusive. The polarization state transition of microglia is intricately linked to neuroinflammation, indicating its crucial involvement in the pathophysiology of depression. Researchers are vigorously pursuing the exploration of this potential treatment strategy, aiming to comprehend its underlying mechanisms. Hence, the current study was designed to investigate the antidepressant mechanisms of PSP via Microglial M1/M2 Polarization, based on the lipopolysaccharide (LPS)-induced BV2 cell activation model. The results indicate that PSP significantly inhibited NO and LDH release and reduced ROS levels in LPS-induced BV2 cells. PSP could significantly reduce the protein expression level of Iba-1, decreased the mRNA levels of TNF-α, IL-1β, and IL-6, and increased the mRNA level of IL-10. PSP also significantly reduced the protein expression level of CD16/32 and increased that of CD206, reduced the mRNA level and fluorescence intensity of iNOS, and increased those of Arg-1. However, PSP pretreatment reversed the alterations of the BDNF/TrkB/CREB and Notch/Hes1 pathways in LPS-induced BV2 cells. These results suggested that PSP exerted the anti-inflammatory effects by inhibiting M1 phenotype polarization and promoting microglia polarization toward the M2 phenotype, and its regulation of microglia M1/M2 polarization may be associated with modulating the BDNF/TrkB/CREB and Notch/Hes1 pathways.
Recent studies have revealed that endophytes in plants can produce metabolites with activity that is comparable to or identical to the host. Dendrobine has attracted much attention in the field of neurodegenerative diseases by exhibiting anti-oxidative stress and neuroprotective effects. This study aimed to investigate the protective effects and mechanisms of metabolites of dendrobium endophytes Pseudomonas protegens CM-YJ44 and Priestia megaterium D-HT207 against H2O2-induced oxidative stress injury in SH-SY5Y cells. Results showed that there were 50 neuroprotective compounds in CM-YJ44 and 72 neuroprotective compounds in D-HT207. Those both increased significantly cell viability, decreased contents of ROS in H2O2-induced SH-SY5Y cells. It was confirmed that metabolites of CM-YJ44 and D-HT207 inhibited the H2O2-induced oxidative stress injury in SH-SY5Y cells, which mechanism is related to inhibition of ROS production, alteration of MMP, and inhibition of apoptosis and inflammatory factors expression via the Nrf2/Keap1 pathway.
The betel nut is one of the most widely consumed addictive substances in the world after nicotine, ethanol, and caffeine. Arecoline is an active ingredient from the areca nut. It has many pharmacological effects and can affect the central nervous system. In this study, we found that arecoline can relieve fatigue behavior. Objective: This research aims to estimate the anti-fatigue effects of arecoline and explore its underlying mechanisms using a murine model of central fatigue precipitated by sleep deprivation (SD). Methods: Seventy-two male C57BL/6 mice were randomly assigned to six groups: a control group, an SD-induced fatigue model group, a group that received Rhodiola Rosea capsules (2.5 mg/kg), and three arecoline groups, which were administered at low, medium, and high doses (10, 20, and 40 mg/kg, respectively). Following 28 days of continuous administrations, the effects of arecoline on mouse fatigue-related behaviors were assessed by behavioral tests, including grip strength, rotarod performance, and weight-bearing swimming endurance. The release levels of the related biochemical markers were measured by enzyme-linked immunosorbent assays (ELISAs). Western blotting was employed to quantify the expression levels of nuclear factor erythroid 2-related factor (Nrf2), Kelch-like ECH-associated protein 1 (Keap1), heme oxygenase 1 (HO-1), sequestosome-1 (p62), and NADPH quinone oxidoreductase 1 (NQO1) in the gastrocnemius muscle. Results: Arecoline administration notably enhanced grip strength, delayed the onset of fatigue as evidenced by extended latencies in rotarod tests, and increased the duration of weight-bearing swimming in mice. In the elevated plus maze, arecoline obviously decreased both the number of entries and the total distance traveled in the open arms. Arecoline markedly decreased the contents of creatine kinase, blood urea nitrogen, lactate dehydrogenase, triglycerides, and cholesterol in the serum, while it elevated the levels of total testosterone, lactate dehydrogenase, and immunoglobulin G. Furthermore, it significantly increased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase in the gastrocnemius muscle, reduced malondialdehyde levels, augmented hippocampal SOD and CAT activity, and elevated glycogen stores in both liver and muscle tissues. Neurotransmitter levels showed significant increases, cytokine levels were markedly reduced, and the expressions of Nrf2, Keap1, NQO1, p62, and HO-1 in brain tissues were significantly upregulated. Conclusions: This study demonstrates that arecoline has anti-fatigue activity, and the specific mechanisms are associated with elevating glucose and lipid metabolism levels, relieving oxidative stress damage, inhibiting neuroinflammatory response, and regulating neurotransmitter levels and the Keap1/Nrf2/HO-1 signaling pathway. The research provides a new direction for arecoline’s potential in preventing and improving fatigue.
Polysaccharides are one of the main active ingredients of Polygonum sibiricum (PS), which is a food and medicine homolog used throughout Chinese history. The antidepressant-like effects of PSP and its underlying mechanisms remain elusive, especially the regulation of microglial polarization. The current study determined the chemical composition and structural characteristics of PSP. Then, the chronic unpredictable mild stress (CUMS) procedure was carried out on the zebrafish for 5 weeks, and PSP was immersed for 9 days (1 h/d). The body weight of zebrafish was monitored, and behavioral tests, including the novel tank test and light and dark tank test, were performed to evaluate the antidepressant-like effects of PSP. Then, the function of the hypothalamic-pituitary-interrenal (HPI) axis, the levels of peripheral inflammation, neuronal and blood–brain barrier damage in the mesencephalon and telencephalon, and the mRNA expression of M1/M2 phenotype genes in the brain were examined. PSP samples had the typical structural characteristics of polysaccharides, consisting of glucose, mannose, and galactose, with an average Mw of 20.48 kDa, which presented porous and agglomerated morphologies. Compared with untreated zebrafish, the depression-like behaviors of CUMS-induced zebrafish were significantly attenuated. PSP significantly decreased the levels of cortisol and pro-inflammatory cytokines and increased the levels of the anti-inflammatory cytokines in the body of CUMS-induced depressive zebrafish. Furthermore, PSP remarkably reversed the neuronal and blood–brain barrier damage in the mesencephalon and telencephalon and the mRNA expression of M1/M2 phenotype genes in the brain. These findings indicated that the antidepressant-like effects of PSP were related to altering the HPI axis hyperactivation, suppressing peripheral inflammation, inhibiting neuroinflammation induced by microglia hyperactivation, and modulating microglial M1/M2 polarization. The current study provides the foundations for future examinations of PSP in the functional foods of emotional regulation.
The purification process and antioxidant activity of flavonoids from P. kingianum Coll. were studied. Through a single factor test combined with a response surface test, ultrasonic-assisted solvent extraction was used to optimize the extraction process of flavonoids from P. kingianum Coll.. Through static and dynamic experiments, the effects of resin type, crude extract concentration, eluent, and elution flow rate on the adsorption and desorption performance of flavonoids from P. kingianum Coll. were investigated, and the best purification conditions were determined. The antioxidant activity of flavonoids from P. kingianum Coll. before and after purification was compared by DPPH free radical and ABTS free radical methods. The results showed that the optimum extraction parameters were ethanol concentration 79%, extraction temperature of 61 ℃, extraction time of 2 h, the ratio of liquid to material 20 mL/g, and the extraction rate reached 0.29%. AB-8 macroporous resin had the best effect on the purification of flavonoids from P. kingianum Coll.. The best condition was that 40 g/L crude extract was put on the column and 70% ethanol was eluted at 2.0 g/L. Under this condition, the purity of flavonoids from P. kingianum Coll. was increased to 5.31%, which was 11.8 times of the concentration of crude extract. The scavenging rates of DPPH and ABTS radicals after purification were 82.44% and 86.22%, which were much higher than those before purification. The study indicates that AB-8 macroporous resin was suitable for separation and purification of flavonoids from P. kingianum Coll. and the flavonoids have antioxidant activity.
The growth of endophytic bacteria is influenced by the host plants and their secondary metabolites and activities. In this study, P. megaterium P-NA14 and P. megaterium D-HT207 were isolated from potato tuber and dendrobium stem respectively. They were both identified as Priestia megaterium. The antimicrobial activities and metabolites of both strains were explored. For antimicrobial activities, results showed that P. megaterium P-NA14 exhibited a stronger inhibition effect on the pathogen of dendrobium, while P. megaterium D-HT207 exhibited a stronger inhibition effect on the pathogen of potato. The supernatant of P. megaterium P-NA14 showed an inhibition effect only on Staphylococcus aureus, while the sediment of P. megaterium D-HT207 showed an inhibition effect only on Escherichia coli. For metabolomic analysis, the content of L-phenylalanine in P. megaterium P-NA14 was higher than that of P. megaterium D-HT207, and several key downstream metabolites of L-phenylalanine were associated with inhibition of S. aureus including tyrosine, capsaicin, etc. Therefore, we speculated that the different antimicrobial activities between P. megaterium P-NA14 and P. megaterium D-HT207 were possibly related to the content of L-phenylalanine and its metabolites. This study preliminarily explored why the same strains isolated from different hosts exhibit different activities from the perspective of metabolomics.