Lycopene Regulates Macrophage Immune Response through the Autophagy Pathway Mediated by RIPK1.

The effects of lycopene (LP) on macrophage immune responses were evaluated in this study. Compared with the control treatment, LP treatment significantly increased cell vitality, phagocytic activity, and chemokine production in RAW264.7 cells. Additionally, compared with the control treatment, 4 µM LP treatment significantly activated autophagy, enhanced mitochondrial membrane potential, and upregulated receptor-interacting protein kinase 1 (RIPK1), while necrostatin-1 significantly reversed these effects of LP. Furthermore, compared with that in the control group, RIPK1 was significantly upregulated in the 4 µM LP and 4 µM LP + spautin-1 groups, whereas p-mTOR levels were reduced. More importantly, compared with that in the control group, p62 was significantly downregulated, and Beclin1, LC3-II, and Atg7 were upregulated in the 4 µM LP group, while spautin-1 significantly reversed these effects of LP. These results confirm that LP activates the mTOR/Beclin1/LC3/p62 autophagy signaling pathway through RIPK1, thereby enhancing the immune response of macrophages.

A role of dentate gyrus mechanistic target of rapamycin activation in epileptogenesis in a mouse model of posttraumatic epilepsy.

OBJECTIVE: The mechanistic target of rapamycin (mTOR) pathway has been implicated in promoting epileptogenesis in animal models of acquired epilepsy, such as posttraumatic epilepsy (PTE) following traumatic brain injury (TBI). However, the specific anatomical regions and neuronal populations mediating mTOR's role in epileptogenesis are not well defined. In this study, we tested the hypothesis that mTOR activation in dentate gyrus granule cells promotes neuronal death, mossy fiber sprouting, and PTE in the controlled cortical impact (CCI) model of TBI. METHODS: An adeno-associated virus (AAV)-Cre viral vector was injected into the hippocampus of Rptorflox/flox (regulatory-associated protein of mTOR) mutant mice to inhibit mTOR activation in dentate gyrus granule cells. Four weeks after AAV-Cre or AAV-vehicle injection, mice underwent CCI injury and were subsequently assessed for mTOR pathway activation by Western blotting, neuronal death, and mossy fiber sprouting by immunopathological analysis, and posttraumatic seizures by video-electroencephalographic monitoring. RESULTS: AAV-Cre injection primarily affected the dentate gyrus and inhibited hippocampal mTOR activation following CCI injury. AAV-Cre-injected mice had reduced neuronal death in dentate gyrus detected by Fluoro-Jade B staining and decreased mossy fiber sprouting by ZnT3 immunostaining. Finally, AAV-Cre-injected mice exhibited a decrease in incidence of PTE. SIGNIFICANCE: mTOR pathway activation in dentate gyrus granule cells may at least partly mediate pathological abnormalities and epileptogenesis in models of TBI and PTE. Targeted modulation of mTOR activity in this hippocampal network may represent a focused therapeutic approach for antiepileptogenesis and prevention of PTE.

Cerebral vascular and blood brain-barrier abnormalities in a mouse model of epilepsy and tuberous sclerosis complex.

OBJECTIVE: Tuberous sclerosis complex (TSC) is a genetic disorder, characterized by tumor formation in the brain and other organs, and severe neurological symptoms, such as epilepsy. Abnormal vascular endothelial growth factor (VEGF) expression may promote angiogenesis in kidney and lung tumors in TSC and has been identified in brain specimens from TSC patients, but the role of VEGF and vascular abnormalities in neurological manifestations of TSC is poorly defined. In this study, we investigated abnormalities in brain VEGF expression, cerebral blood vessel anatomy, and blood-brain barrier (BBB) structure and function in a mouse model of TSC. METHODS: Tsc1GFAP CKO mice were used to investigate VEGF expression and vascular abnormalities in the brain by Western blotting and immunohistochemical analysis of vascular and BBB markers. In vivo two-photon imaging was used to assess BBB permeability to normally impenetrable fluorescently labeled compounds. The effect of mechanistic target of rapamycin (mTOR) pathway inhibitors, VEGF receptor antagonists (apatinib), or BBB stabilizers (RepSox) was assessed in some of these assays, as well as on seizures by video-electroencephalography. RESULTS: VEGF expression was elevated in cortex of Tsc1GFAP CKO mice, which was reversed by the mTOR inhibitor rapamycin. Tsc1GFAP CKO mice exhibited increased cerebral angiogenesis and vascular complexity in cortex and hippocampus, which were reversed by the VEGF receptor antagonist apatinib. BBB permeability was abnormally increased and BBB-related tight junction proteins occludin and claudin-5 were decreased in Tsc1GFAP CKO mice, also in an apatinib- and RepSox-dependent manner. The BBB stabilizer (RepSox), but not the VEGF receptor antagonist (apatinib), decreased seizures and improved survival in Tsc1GFAP CKO mice. SIGNIFICANCE: Increased brain VEGF expression is dependent on mTOR pathway activation and promotes cerebral vascular abnormalities and increased BBB permeability in a mouse model of TSC. BBB modulation may affect epileptogenesis and represent a rational treatment for epilepsy in TSC.

Spatial and amplitude dynamics of neurostimulation: Insights from the acute intrahippocampal kainate seizure mouse model.

OBJECTIVE: Neurostimulation is an emerging treatment for patients with drug-resistant epilepsy, which is used to suppress, prevent, and terminate seizure activity. Unfortunately, after implantation and despite best clinical practice, most patients continue to have persistent seizures even after years of empirical optimization. The objective of this study is to determine optimal spatial and amplitude properties of neurostimulation in inhibiting epileptiform activity in an acute hippocampal seizure model. METHODS: We performed high-throughput testing of high-frequency focal brain stimulation in the acute intrahippocampal kainic acid mouse model of status epilepticus. We evaluated combinations of six anatomic targets and three stimulus amplitudes. RESULTS: We found that the spike-suppressive effects of high-frequency neurostimulation are highly dependent on the stimulation amplitude and location, with higher amplitude stimulation being significantly more effective. Epileptiform spiking activity was significantly reduced with ipsilateral 250 µA stimulation of the CA1 and CA3 hippocampal regions with 21.5% and 22.2% reductions, respectively. In contrast, we found that spiking frequency and amplitude significantly increased with stimulation of the ventral hippocampal commissure. We further found spatial differences with broader effects from CA1 versus CA3 stimulation. SIGNIFICANCE: These findings demonstrate that the effects of therapeutic neurostimulation in an acute hippocampal seizure model are highly dependent on the location of stimulation and stimulus amplitude. We provide a platform to optimize the anti-seizure effects of neurostimulation, and demonstrate that an exploration of the large electrical parameter and location space can improve current modalities for treating epilepsy. PLAIN LANGUAGE SUMMARY: In this study, we tested how electrical pulses in the brain can help control seizures in mice. We found that the electrode's placement and the stimulation amplitude had a large effect on outcomes. Some brain regions, notably nearby CA1 and CA3, responded positively with reduced seizure-like activities, while others showed increased activity. These findings emphasize that choosing the right spot for the electrode and adjusting the strength of electrical pulses are both crucial when considering neurostimulation treatments for epilepsy.

Streptomyces changanensis sp. nov. Isolated from Soil in China.

An aerobic, Gram-positive, and non-motile actinomycete, designated HL-66 T, was isolated from a soil sample collected in the Meridian Valley, Shaanxi Province, China. Morphological, chemotaxonomic, and phylogenetic characteristics showed a high similarity to the genus Streptomyces. Based on 16S rRNA gene sequence analysis, the closest phylogenetic neighbour of HL-66 T were Streptomyces lavendofoliae NBRC 12882 T (99.17%), Streptomyces gobitricini NBRC 15419 T (99.03%) and Streptomyces roseolilacinus NBRC 12815 T (98.96%). Genome relatedness indexes revealed that the average nucleotide identity and digital DNA-DNA hybridization values between HL-66 T and its closest phylogenomic relative (S. roseolilacinus JCM 4335 T) were 88.61% and 32.10%, respectively. The cell-wall peptidoglycan contains LL-diaminopimelic acid. Predominant menaquinones are MK-9 (H6), MK-9(H4) and MK-9(H8). The major cellular fatty acids were iso-C16:0, anteiso-C15:0, iso-C16:1 H, and C16:1 ω7c. The polar lipid pattern consisted of diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylinositol, phosphatidylinositol mannosides, and an unknown phospholipid. Based on phylogenetic analyses, genome-genome distance calculation, and average nucleotide identity, strain HL-66 T represents a novel species of the genus Streptomyces. Therefore, a new species Streptomyces changanensis sp. nov. is proposed with strain HL-66 T (= CGMCC 22674 = JCM 35800) as the type strain.

Protective effect of vitamin C against tetrachlorobenzoquinone-induced 5-hydroxymethylation-dependent apoptosis in HepG2 cells mainly via the mitochondrial apoptosis pathway.

Tetrachlorobenzoquinone (TCBQ) is an active metabolite of pentachlorophenol, and stimulates the accumulation of ROS to trigger apoptosis. The preventive effect of vitamin C (Vc) against TCBQ-induced apoptosis in HepG2 cells is unknown. And there is little known about TCBQ-triggered 5-hydromethylcytosine (5hmC)-dependent apoptosis. Here, we confirmed that Vc alleviated TCBQ-induced apoptosis. Through investigating the underlying mechanism, we found TCBQ downregulated 5hmC levels of genomic DNA in a Tet-dependent manner, with a particularly pronounced decrease in the promoter region, using UHPLC-MS-MS analysis and hydroxymethylated DNA immunoprecipitation sequencing. Notably, TCBQ exposure resulted in alterations of 5hmC abundance to ∼91% of key genes at promoters in the mitochondrial apoptosis pathway, along with changes of mRNA expression in 87% of genes. By contrast, 5hmC abundance of genes only exhibited slight changes in the death receptor/ligand pathway. Interestingly, the pretreatment with Vc, a positive stimulator of 5hmC generation, restored 5hmC in the genomic DNA to near-normal levels. More notably, Vc pretreatment further counter-regulated TCBQ-induced alteration of 5hmC abundance in the promoter with 100% of genes, accompanying the reverse modulation of mRNA expressions in 89% of genes. These data from Vc pretreatment supported the relationship between TCBQ-induced apoptosis and the altered 5hmC abundance. Additionally, Vc also suppressed TCBQ-stimulated generation of ROS, and further increased the stability of mitochondria. Our study illuminates a new mechanism of TCBQ-induced 5hmC-dependent apoptosis, and the dual mechanisms of Vc against TCBQ-stimulated apoptosis via reversely regulating 5hmC levels and scavenging ROS. The work also provided a possible strategy for the detoxification of TCBQ.

Spatial and Amplitude Dynamics of Neurostimulation: Insights from the Acute Intrahippocampal Kainate Seizure Mouse Model.

Objective: Neurostimulation is an emerging treatment for patients with medically refractory epilepsy, which is used to suppress, prevent, and terminate seizure activity. Unfortunately, after implantation and despite best clinical practice, most patients continue to have persistent seizures even after years of empirical optimization. The objective of this study is to determine optimal spatial and amplitude properties of neurostimulation in inhibiting epileptiform activity in an acute hippocampal seizure model. Methods: We performed high-throughput testing of high-frequency focal brain stimulation in the acute intrahippocampal kainic acid mouse model of temporal lobe epilepsy. We evaluated combinations of six anatomic targets and three stimulus amplitudes. Results: We found that the spike-suppressive effects of high-frequency neurostimulation are highly dependent on the stimulation amplitude and location, with higher amplitude stimulation being significantly more effective. Epileptiform spiking activity was significantly reduced with ipsilateral 250 µA stimulation of the CA1 and CA3 hippocampal regions with 21.5% and 22.2% reductions, respectively. In contrast, we found that spiking frequency and amplitude significantly increased with stimulation of the ventral hippocampal commissure. We further found spatial differences with broader effects from CA1 versus CA3 stimulation. Significance: These findings demonstrate that the effects of therapeutic neurostimulation in an acute hippocampal seizure model are highly dependent on the location of stimulation and stimulus amplitude. We provide a platform to optimize the anti-seizure effects of neurostimulation, and demonstrate that an exploration of the large electrical parameter and location space can improve current modalities for treating epilepsy. Key Points: Evaluated spatial and temporal parameters of neurostimulation in a mouse model of acute seizuresBrief bursts of high-frequency (100 Hz) stimulation effectively interrupted epileptiform activity.The suppressive effect was highly dependent on stimulation amplitude and was maximal at the ipsilateral CA1 and CA3 regions.Pro-excitatory effects were identified with high-amplitude high-frequency stimulation at the ventral hippocampal commissure and contralateral CA1.

HpaII-assisted and linear amplification-enhanced isothermal exponential amplification fluorescent strategy for rapid and sensitive detection of DNA methyltransferase activity.

The detection of methyltransferase (MTase) activity is of great significance in methylation-related disease diagnosis and drug screening. Herein, a HpaII-assisted and linear amplification-enhanced exponential amplification strategy is proposed for sensitive and label-free detection of M.SssI MTase activity. The P1 probe contains self-complementary sequence 5'-CTAGCCGGCTAG-3' at 3'-terminal. After denaturation and annealing, P1 probes hybridize with itself to generate P1 duplexes. M.SssI MTase induces methylation of cytosine at 5'-CG-3' in P1 duplexes, and thus, HpaII fails to cleave at 5'-CCGG-3' due to methylation sensitivity, leaving P1 duplex intact. Then, these intact P1 duplexes are extended along 3'-terminal through Vent (exo-) DNA polymerase to generate dsDNA, which is recognized and nicked at the recognition sites by Nt.BstNBI, releasing two copies of primer X. Primer X hybridizes with X' at the amplification template T1 (X'-Y'-X') and then serves as primers to trigger the exponential amplification reaction (EXPAR). The point of inflection (POI) values of real-time fluorescence curves is linearly correlated with the logarithm of M.SssI MTase concentration in the range of 0.125 [Formula: see text] 8 U mL-1 with a low detection limit of 0.034 U mL-1. In the absence of M.SssI, P1 duplexes are cut by HpaII and separated into ssDNA under the executed temperature of EXPAR and thus unable to trigger the amplification. The strategy provides good selectivity against other types of MTases and protein and is able to detect M.SssI activity in human serum. Furthermore, the analytical method has the generality and can be extended to the analysis of other types of DNA MTases.

Structural characterization and induction of tumor cell apoptosis of polysaccharide from purple sweet potato (Ipomoea batatas (L.) Lam).

The carbohydrate is the main ingredient of purple sweet potato. A polysaccharide, named PSP, was separated and purified from purple sweet potato by extraction with hot water, precipitation with ethanol, deproteinization with Sevag reagent and column chromatography with Sephadex G-100. The purity and structure were studied with HPLC, UV-Vis, GC-MS and NMR. The PSP is a neutral polysaccharide with Mw of 470 kDa. The monosaccharide composition of PSP contained D-xylose, d-glucose, D-galactose with ratio of 1.0: 8.3: 1.3. The backbone of PSP was composed of the residues of →6)-D-Glcp-(1 â†’ and →2, 6)-D-Glcp-(1→. The branches of PSP contained the residues of →3)-D-Galp-(1→, and D-Xylp-(1→. The antitumor activity in vitro of PSP was analyzed with HT-29 cells. And the SEM, AO staining, MDC staining and hoechst 33342 staining were performed to study the effect on apoptosis of HT-29 cells by PSP. The results revealed that the PSP can significantly inhibit the proliferation of HT-29 cells from induction apoptosis. The manuscript provided valuable knowledges on structural characteristics of the polysaccharides from purple sweet potato.

The role of the ferroptosis pathway in the regulation of polysaccharides for human health: A review.

Polysaccharides are natural polymers with ketone or aldehyde groups that are widely found in plants, animals, and microorganisms. They exhibit various biological activities and have potential development value in the food and pharmaceutical fields. Ferroptosis is a recently discovered modality that modulates cell death and has attracted considerable attention because it is considered to be involved in many pathophysiological processes. The inhibition of ferroptosis by reducing intracellular iron accumulation and lipid peroxidation may provide potential protective strategies against related pathologies. Ferroptosis is also involved in the physiological activities of polysaccharides, and its regulatory mechanism varies according to different physiological activities. However, a systematic summary on the involvement of ferroptosis in the physiological activities of polysaccharides is currently lacking. Therefore, this review systematically summarized the relationship between the physiological activities of polysaccharides and ferroptosis and focused on the regulatory mechanism of ferroptosis, with respect to the anti-cancer, anti-inflammatory, antioxidant, and immunomodulatory activities of all polysaccharides. The primary objective was to find new polysaccharide-related therapeutic breakthroughs for related diseases and to provide a reference for further research on polysaccharides-based therapeutics.

A polysaccharide from Pleurotus citrinopileatus mycelia enhances the immune response in cyclophosphamide-induced immunosuppressed mice via p62/Keap1/Nrf2 signal transduction pathway.

The manuscript aimed to study the immunoregulatory activity and the mechanism of the polysaccharide (CMP) from Pleurotus citrinopileatus mycelia. The mice were divided into normal group, model group, different dosage of CMP (50, 100 and 200 mg/kg, respectively) groups and levamisole hydrochloride treated group. The results showed that, compared with the model group, CMP could significantly improve the auricle swelling rate, half hemolysis value and phagocytic index in mice. The indices of immune organs were raised, and tissue damage of spleen was relieved. Splenic Th1 cells were decreased, while Th2 cells were increased, furthermore the proliferation of splenic lymphocytes and the cytotoxicity of NK cells were increased. The levels of interleukin-12 (IL-12), interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) in spleen were decreased, while interleukin-4 (IL-4) and interleukin-10 (IL-10) were increased. In serum and spleen, the levels of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities were increased, while the level of malondialdehyde (MDA) was decreased. And the levels of Immunoglobulin were also increased. Western blot showed that CMP had immunoregulatory activity by activating Nrf2, Keap1, p62, HO-1, and NQO1 in the p62/Keap1/Nrf2 signaling pathway. The study proved that CMP could be used as a biological Immune regulating agent.

What Drives Visitors' Use of Bins in Urban Parks? An Application of the Stimulus-Organism-Response Model.

Littering by visitors has led to severe challenges for rubbish collection in urban parks. One way to solve this problem is to encourage visitors to put rubbish in the bin. The purpose of this study is to explore the mechanism that drives people's use of bins in urban parks. The theoretical model of stimulus-organism-response is used to test the influence of stimuli (personal and social norms) on people's psychology (facilitators and inhibitors), thereby producing responses (the use of bins). In this study, we used a purposeful sampling method. Overall, 400 questionnaires were distributed, and 356 valid questionnaires were collected from visitors to the Shanghai City Park in China. The data were analysed using structural equations. The results show that personal and social norms have a significant impact on visitors' internal psychological state (facilitators and inhibitors). More specifically, personal and social norms are positively correlated with facilitators and negatively correlated with inhibitors. They have a significant positive impact on people's use of bins. We also found that facilitators and inhibitors partially mediate the relationship between norms and behaviours. The study suggests park managers should introduce various measures to influence people's personal norms and cultivate people's awareness of their obligation, responsibility, and commitment to the environment, and managers should also show visitors the consequences of not properly disposing of their rubbish as well as place more rubbish bins in key areas.

Preventive Mechanism of Lycopene on Intestinal Toxicity Caused by Cyclophosphamide Chemotherapy in Mice by Regulating TLR4-MyD88/TRIF-TRAF6 Signaling Pathway and Gut-Liver Axis.

Cyclophosphamide (CYC) is the first-line chemotherapy drug for cancer in clinical practice, and its intestinal toxicity seriously affects the treatment effect and prognosis of patients. Lycopene (LP) is the main pigment of ripe tomatoes and has strong antioxidant activity. However, the mechanism by which LP prevents CYC-induced intestinal injury remains unclear. The aim of this study was to investigate the mechanism of LP in preventing intestinal toxicity caused by CYC chemotherapy in mice. The results showed that LP significantly prevented spleen and thymus atrophy induced by CYC. In terms of intestinal injury, LP significantly increased the levels of superoxide dismutase (SOD), secretory immunoglobulin A (sIgA), interleukin (IL)-4, IL-12, and interferon (IFN)-γ, decreased the content of lipid oxidation (MDA), upregulated the protein expressions of toll-like receptors 4 (TLR4), myeloid differentiation factor 88 (MyD88), tumor necrosis factor receptor-associated factor 6 (TRAF6), toll/IL-1receptor domain containing adaptor protein inducing IFN-ß (TRIF), p-P38 MAPK (P38), and p-nuclear factor kappa-B (NF-κB) p65, and improved the small intestine tissue injury induced by CYC. In terms of liver injury, LP significantly increased the content of glutathione (GSH), decreased the contents of MDA, nitric oxide (NO), IL-1ß, IL-6, and tumor necrosis factor (TNF)-α, and repaired the liver tissue injury induced by CYC. Importantly, 10 mg/kg LP significantly prevented intestinal microbiota dysregulation in CYC mice. These results suggested that LP significantly prevented intestinal injury induced by CYC in mice by regulating the TLR4-MyD88/TRIF-TRAF6 signaling pathway and gut-liver axis.

Roles of the EPS66A polysaccharide from Streptomyces sp. in inducing tobacco resistance to tobacco mosaic virus.

EPS66A was derived from an unidentified Streptomyces sp. HL-66 by chemical fraction and disease-resistance assays. It was identified as a polysaccharide through a series of chemical characterization, including infrared spectrum analysis, methylation, gas chromatography-mass spectrometry, nuclear magnetic resonance, and high-performance gel permeation chromatography. To determine its effect in plant, EPS66A was applied to tobacco leaves infected with TMV, resulting in the plant with enhanced systemic resistance with a significant reduction of TMV severity. Plant defense was confirmed by early responses, including hypersensitive response (HR) indicated by programed cell death, moderate alkalization, oxidative burst, increase in nitric oxide (NO) and salicylic acid (SA). Furthermore, EPS66A induced callose deposition to form defense barriers against pathogen invasion and the expression of pathogenesis-related (PR) genes, which confirmed the second level of plant defense. Therefore, EPS66A served as a resistance inducer, which was reorganized by tobacco cells that triggered the production of signal molecules. The signals moved in long distance and systemically in plant, which coordinated the expression of defense responses. The study provided a new perspective in understanding the mechanism of EPS66A in regulating plants on environmental adaptability and provided a theoretical foundation for designing safe and sustainable pesticides.

Effects of indole derivatives from Purpureocillium lilacinum in controlling tobacco mosaic virus.

There are various types of compounds studied and applied for plant disease management, and some of them are environment friendly and suitable in organic production. An example is indole-3-carboxaldehyde (A1) and indole-3-carboxylic acid (A2) derived from Purpureocillium lilacinum H1463, which have shown a strong activity in the control of tobacco mosaic virus (TMV). In this study, the effects of these compounds were studied on suppressing TMV and corresponding mechanism. Both A1 and A2 exhibited strong anti-TMV activities in vitro and in vivo. They fractured TMV virions and forced the fractured particles agglomerated. A1 and A2 also induced immune responses or resistance of tobacco to TMV infection, including expressing hypersensitive reaction (HR), increasing defense-related enzymes and overexpressing pathogenesis-related (PR) proteins. The upregulation of salicylic acid (SA) biosynthesis genes PAL, ICS, and PBS3 confirmed that SA served as a defense-related signal molecule. Therefore, indole derivatives have a potential for activating defense of tobacco against TMV and other pathogens and can be used for disease control.

An Impact Asymmetry Analysis of Small Urban Green Space Attributes to Enhance Visitor Satisfaction.

Urban green spaces have beneficial effects on the health and well-being of citizens. Understanding the factors influencing visitor satisfaction with urban green spaces contributes to making more informed policies. Prior studies on green spaces satisfaction primarily focused on the linear correlation between small urban green space attributes and satisfaction. In this manuscript, we presented a study aimed to (1) identify the attributes of SUGS as frustrators, dissatisfiers, hybrids, satisfiers, and delighters; (2) prioritize attributes for effective satisfaction management; (3) assist managers in drafting guidelines for operational management decisions. We gathered a range of information about the users to nine SUGS in Shanghai, in 2020, via a questionnaire, and we found that safety, noise, and social interaction are improvement priorities. Squares and visitors' behavior should not be ignored in SUGS management. Moreover, managers should carefully monitor SUGS attributes of the social environment to meet users' expectations. The findings of this study have implications for SUGS management and future research.

Preventive Effect of Lycopene in Dextran Sulfate Sodium-Induced Ulcerative Colitis Mice through the Regulation of TLR4/TRIF/NF-κB Signaling Pathway and Tight Junctions.

The preventive effect and molecular mechanism of lycopene (LP) in dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice were evaluated. Compared to the DSS group, the LP prevention groups not only significantly inhibited the DSS-induced weight loss, decreased the disease activity index (DAI) score, increased the colon length, and improved inflammation in the colon but also significantly increased the levels of superoxide dismutase (SOD),catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione (GSH) in the colon and reduced inflammatory cytokine, myeloperoxidase (MPO), and malondialdehyde (MDA) levels. Notably, when compared to the DSS group, the protein expression levels of TLR4, TRIF, and p-NF-κB p65 in the mice colon tissue were downregulated and those of tight junction-related proteins were upregulated in the LP + DSS group, with the most significant effect observed in the 10 mg/kg LP + DSS group. These results confirmed that the upregulation of tight junction-related protein expression after blocking the TLR4/TRIF/NF-κB signaling pathway may be one of the mechanisms through which LP prevents UC.

Breast-Feeding is Not a Risk Factor of Mother-to-Child Transmission of Hepatitis B Virus.

PURPOSE: This study aims at researching the content of hepatitis B virus (HBV) DNA in the breast milk of the mothers carrying HBV and investigating the effects of different feeding methods on mother-to-child transmission (MTCT) of HBV. METHODS: All infants were voluntarily chosen by their mothers and divided into breast-feeding group and formula-feeding group, which were divided into three subgroups, respectively: HBV-DNA negative (HBV-) group, low viral load (LVL) group and high viral load (HVL) group. RESULTS: HBV load in colostrum and mature milk were both significantly lower than in serum (P < 0.001). The positive rate of HBV-DNA in colostrum was positively correlated with HBV load in serum, significantly higher than that of the HBV-Group in colostrum in the LVL Group (P < 0.05), and the HVL Group was significantly higher than the LVL Group (P < 0.001). The analysis of risk factors of HBV infection in infants showed that breast-feeding and HBsAg positive in colostrum did not increase the risks of HBV infection of infants (P > 0.05). CONCLUSION: Breast-feeding is safe for infants with HBV-infected mothers who receive active immunization combined with passive immunization. As well, breast-feeding will neither increase the risks of HBV infection for infants nor weaken their immunity to HBV. However, breast-feeding shall be cautiously applied to pregnant women with high viral load.

Polysaccharides in natural products that repair the damage to intestinal mucosa caused by cyclophosphamide and their mechanisms: A review.

Cyclophosphamide (CTX) is a commonly used antitumor drug in clinical practice, and intestinal mucosal injury is one of its main toxic side effects, which seriously affects the treatment tolerance and prognosis of patients. Therefore, the prevention of intestinal mucosal injury is a research hotspot. Studies have shown that polysaccharides can effectively prevent and improve CTX-induced intestinal mucosal injury and immune system disorders. Recent research has elucidated the structure, biological function, and physicochemical properties of polysaccharides that prevent intestinal mucosal injury, and the potential mechanisms whereby they have this effect. In this paper, we review the recent progress made in understanding the effects of polysaccharides on intestinal mucosal injury and their protective mechanism in order to provide a reference for further research on the prevention of intestinal mucosal injury and the mechanisms involved in nutritional intervention.

H2O2 signaling modulates Glycoprotein-1 induced programmed cell death in tobacco suspension cells.

Glycoprotein (GP)-1 is a glycoprotein elicitor with antiviral activity found in Streptomyces kanasensis zx01. GP-1 can induce programmed cell death (PCD) in vitro; however, the underlying mechanism is unclear. In the present study, we demonstrated that GP-1 induced PCD in tobacco suspension cells, which was modulated by hydrogen peroxide (H2O2). GP-1 participated in and modulated biologically relevant signaling in plant cells. GP-1 induced tobacco cell death in a dose- and time-dependent manner; affected the expression of BRI1-associated receptor kinase 1 (BAK1) and the accumulation of salicylic acid (SA), which are related to PCD; and enzymatic activities and mitochondrial functions. In conclusion, GP-1-induced PCD in tobacco may be mediated by H2O2 which alters BAK1 and SA levels, as well as mitochondrial and gene function. This cell signal cascade played an important role in the process of GP-1 induced plant disease resistance.