Charantia Polysaccharides Research Articles

Microcapsule Preparation and Properties of Flavonoid Extract from Immature Citrus reticulata 'Chachiensis' Peel.

Citrus reticulata 'Chachiensis' is a citrus cultivar in the Rutaceae family, and its peel is commonly utilized as a raw material for Guangchenpi. This study used flavonoid extract from the peel of immature Citrus reticulata 'Chachiensis' (CCE) as the raw material to investigate the encapsulation ability of different wall materials (plant-based proteins, including soybean protein isolation (SPI), pea protein (PP), and zein; carbohydrates, including maltodextrin (MD), Momordica charantia polysaccharide (MCP), and gum acacia (GA); and composite wall materials of both types) on CCE. The wall material with the highest encapsulation rate was selected for the preparation of CCE microcapsules. Furthermore, the physicochemical characteristics, antioxidant capacity, bioavailability, and storage stability of the CCE microcapsules were explored. The results indicated that among all wall materials, the composite wall material PPMD had the highest encapsulation rate, which was 84.44 ± 0.34%. After encapsulation, the microcapsules tended to have a yellow color and exhibited characteristics such as system stability, low moisture content, and low hygroscopicity. In vitro antioxidant assays revealed that the encapsulation of CCE significantly increased the scavenging rates of DPPH and ABTS free radicals. In vitro gastrointestinal digestion experiments indicated that the release rate of PPMD-CCE in intestinal fluid was significantly greater than that of free CCE, ultimately reaching 85.89 ± 1.53%. Storage experiments demonstrated that after 45 days under various temperature and light conditions, the retention rate of CCE in the microcapsules was significantly greater than that of free CCE. The above findings provide new possibilities for the application of PP and plant proteins and lay a foundation for the future industrial application of CCE.

Momordica charantia Polysaccharide intervention ameliorates the symptoms of dextran sulfate sodium (DSS)-induced colitis by modulating gut microbiota and inhibiting inflammation

Momordica Charantia Polysaccharide (MCP), the main active ingredient of M. charantia, exhibits multiple pharmacological properties. However, its effects and mechanisms against ulcerative colitis (UC) remain unclear. In this study, we employed a dextran sulfate sodium (DSS)-induced experimental colitis model to investigate the therapeutic potential of MCP. Our results revealed that prophylactic MCP dramatically attenuated the pathological symptoms associated with colitis in mice, including body weight loss, reduction in colon length, and tissue damage. Moreover, we found prophylactic MCP reduced DSS-induced intestinal permeability and enhanced intestinal barrier integrity. Notably, we observe that prophylactic MCP restored the diversity and richness of the gut microbiota, thereby ameliorating gut microbiota dysbiosis in DSS-induced mice models. Furthermore, fecal microbiota transplantation (FMT) experiments demonstrated that the microbiota derived from MCP-dosed mice remarkably alleviated colitis symptoms. Collectively, our study provided valuable insights into the potential of MCP as a promising prebiotic agent for maintaining intestinal health, and demonstrated that MCP ameliorated colitis in a gut microbiota-dependent manner.

Protective effects and mechanisms of Momordica charantia polysaccharide on early-stage diabetic retinopathy in type 1 diabetes

Momordica charantia polysaccharide (MCP) is a potential drug for the prevention and alleviation of diabetes mellitus (DM) and diabetic retinopathy (DR). This study aimed to investigate the potential protective effects of MCP on early-stage DR and explore the underlying mechanisms. The model group (DM group) and treatment group (D+H group) were established by inducing type 1 DM using a single dose of streptozotocin (STZ) at 60 mg/kg. After modeling, the D+H group was orally administered a 500 mg/kg dose of MCP solution once daily for 12 weeks. Monitoring of systemic indicators (FBG, body weight, general condition) and retinal tissue inflammation and apoptosis (HE staining, IL-6, MCP-1, TNF-α, VEGF, NF-κB, Caspase-3) in this study demonstrated that MCP intervention alleviated both DM and DR. MCP improved the body weight and general condition of DM rats by reducing FBG levels. It also enhanced the anti-inflammatory and anti-apoptotic capabilities of retinal neurons and microvessels by modulating the actions of cytokines, thereby further regulating the inflammation and apoptosis of retinal neurons and microvessels. The underlying mechanisms may be associated with the downregulation of NF-κB and Caspase-3 pathway protein expression, as well as the downregulation of mRNA expression of NF-κB and Caspase-3 pathway genes. Further research is needed to elucidate the potential mechanisms underlying the protective effects of MCP on DR. MCP may emerge as a selective medication for the prevention and alleviation of DM and a novel natural medicine for the prevention and alleviation of DR.

Effect of Momordicacharantia polysaccharide on immunomodulatory activity in mice.

Momordica charantia polysaccharides (MCPs) have been reported to exert beneficial roles, such as disease healing, in medicine and pharmacy. However, little is known about their effects on immunomodulation. The present study aimed to explore the possible effects of Momordica charantia polysaccharide (MCP) on the immunomodulatory activity of mice lymphocytes. To this aim, male BALB/c mice aged 6-8 weeks were assigned to the following six experimental groups: i) Normal (NG); ii) model (MG); iii) positive (PG); iv) MCP low-dose (MLG); v) MCP medium-dose (MMG); and vi) MCP high-dose (MHG). An immunosuppressive model was established by the intraperitoneal injection of cyclophosphamide in all groups apart from NG. The NG and MG mice were fed with distilled water, whereas the PG mice were administered with levamisole and the MLG, MMG and MHG mice were fed on low, medium and high (100, 200 and 300 mg/kg, respectively) doses of MCP for 21 consecutive days. Subsequently, the mice underwent surgical procedure and were analysed using a range of procedures, including measurement of the thymus index (TI) and spleen index (SI), assessment of the lymphocyte proliferation rate and cell phagocytosis of peritoneal macrophages, lymphocyte proliferation, secretion and mRNA expression of cytokines IFN-γ, IL-6 and IL-12. The mice divided into six groups as mentioned above and treated for 7 days, in the first 6 days, except NG group, mice in each group were desiccated in the abdominal cavity and sensitized by 1% dinitrofluorobenzene (DNFB). On day 6, mice were sensitized with 20 µl DNFB/acetone/olive oil solution behind the right ear and in front of the right ear. Compared with those in the NG mice (not injected with 80 mg/kg cyclophosphamide), the TIs and SIs of the PG, MLG, MMG and MHG mice were increased. In addition, the inhibitory rate of ear swelling and the phagocytic activity of peritoneal macrophages in the PG, MLG, MMG and MHG mice were increased compared with those of MG. Furthermore, the lymphocyte proliferation rate, the secretion and relative mRNA expression levels of cytokines IFN-γ, IL-6 and IL-12 were significantly increased in the PG, MMG and MHG mice compared with those in the NG mice. The results from the present study suggest that treatment with MCP led to an upregulation of the organ indices of immunosuppressed mice, reduced their delayed allergic reaction indicated by the differential cytokine levels, improved the phagocytic activity of peritoneal macrophages, enhanced the proliferation rate of lymphocytes, increased the secretion and expression of IFN-γ, IL-6 and IL-12. Therefore, MCP may improve the immune function of the immunosuppressed mice.

Momordica charantia polysaccharide ameliorates D-galactose-induced aging through the Nrf2/β-Catenin signaling pathway.

Aging is widely thought to be associated with oxidative stress. Momordica charantia (MC) is a classic vegetable and traditional herbal medicine widely consumed in Asia, and M. charantia polysaccharide (MCP) is the main bioactive ingredient of MC. We previously reported an antioxidative and neuroprotective effect of MCP in models of cerebral ischemia/reperfusion and hemorrhage injury. However, the role played by MCP in neurodegenerative diseases, especially during aging, remains unknown. In this study, we investigated the protective effect of MCP against oxidative stress and brain damage in a D-galactose-induced aging model (DGAM). The Morris water maze test was performed to evaluate the spatial memory function of model rats. The levels of malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) were measured and telomerase activity was determined. The results showed that MCP treatment attenuated spatial memory dysfunction induced by D-galactose. In addition, MCP increased antioxidant capacity by decreasing MDA and increasing SOD and GSH levels. MCP treatment also improved telomerase activity in aging rats. Mechanistically, MCP promoted the entry of both Nrf2 and β-Catenin into the nucleus, which is the hallmark of antioxidation signaling pathway activation. This study highlights a role played by MCP in ameliorating aging-induced oxidative stress injury and reversing the decline in learning and memory capacity. Our work provides evidence that MCP administration might be a potential antiaging strategy.

Momordica charantia polysaccharides alleviate diarrhea-predominant irritable bowel syndrome by regulating intestinal inflammation and barrier via NF-κB pathway.

Momordica charantia exerts anti-inflammatory effect against ulcerative colitis. Momordica charantia polysaccharides (MCPs) attenuate gastritis through inhibition of ethanol-induced inflammatory response. The role of MCPs in diarrhea-predominant irritable bowel syndrome (IBS-D) is investigated. Chemical stimulation followed by acute and chronic pressure stimulation was used to establish rats model with IBS-D. The model rats were then administrated with MCPs. Defecation frequency, fecal water content and abdominal withdrawal reflex (AWR) score were then recorded. Pathologic changes in the colonic tissues were evaluated by hematoxylin and eosin staining. Inflammation was detected by ELISA and qRT-PCR, and immunohistochemistry was used to assess intestinal mucosal permeability. First, IBS-D of mice wasIBS-D ratsmice exhibited many abnormal clinical manifestations, including increased frequency of defecation, fecal water content, and abdominal withdrawal reflex (AWR) score. Second, the mice were administrated with MCPs, which reduced frequency of defecation, fecal water content, and AWR score, and 100-mg/kg MCPs indicated therapeutic effect on IBS-D mice equivalent to rifaximin. Moreover, MCPs also ameliorated pathologic changes in the colonic tissues of IBS-D mice. Third, inflammatory response in IBS-D mice was also suppressed by MCPs through up-regulation of Interleukin (IL)-10, and down-regulation of tumor necrosis factor-α (TNF-α), Interleukin(IL)-1β, and IL-6. MCPs enhanced levels of occludin (OCLN) and zona occludens protein-1 (ZO-1) in IBS-D mice to improve intestinal mucosal permeability. Finally, phosphorylation of p65 in IBS-D mice was reduced by MCP treatment. MCPs ameliorated intestinal permeability and repressed intestinal inflammation to attenuate IBS-D by inactivating nuclear factor kappa B (NF-κB) signaling.

Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway

Objective. To investigate the potential role of Momordica charantia polysaccharides (MCPs) in Parkinson’s disease (PD) and reveal the molecular mechanism of its function. Method. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (1-methyl-4-phenylpyridinium, MPP+) were used to establish PD mice and cell models. The mice and cells were divided into 4 groups: Control group, Control+MCPs group, PD group, and PD+MCPs group. Pole climbing experiment and Rotarod experiment were used to observe the coordination ability of mice. High-performance liquid chromatography and enzyme-linked immunosorbent assay (ELISA) were used to determine neurotransmitters and metabolites, inflammatory factors TNF-α and IL-1β, oxidative stress-related markers SOD, MDA, and GSH in striatum tissues. Western blot was used to determine the protein levels of tyrosine hydroxylase (TH), oxidative stress-related protein Cytochrome C (Cytochrome C), and apoptosis-related proteins Bcl-2, Bax, and cleaved Caspase-3 in tissues and cells. Moreover, flow cytometry, PI staining, and fluorescence were used to observe cell apoptosis. Finally, the activation effect of MCPs on TLR4/MyD88/NF-κB signaling pathway was observed and verified. Results. Compared with the Control group, MPTP treatment can induce brain damage in mice (all P < 0.05 ), change the metabolic state of neurotransmitters (all P < 0.05 ), induce inflammation (all P < 0.05 ), and induce apoptosis and the occurrence of oxidation reaction (all P < 0.05 ); however, MCPs treatment can significantly reverse the above changes (all P < 0.05 ). In cell models, studies have found that MCPs can play a protective role by regulating the activation state of TLR4/MyD88/NF-κB pathway. Conclusion. This study found that the application of MCPs therapy can play anti-inflammatory, antioxidative stress, and antiapoptotic effects in PD by regulating the activation of the TLR4/MyD88/NF-κB pathway.

Promotion of Momordica Charantia polysaccharides on neural stem cell proliferation by increasing SIRT1 activity after cerebral ischemia/reperfusion in rats

The deacetylase SIRT1 has been reported to play a critical role in regulating neurogenesis, which may be an adaptive processes contributing to recovery after stroke. Our previous work showed that the antioxidant capacity of Momordica charantia polysaccharides (MCPs) could protect against cerebral ischemia/reperfusion (I/R) after stroke. However, whether the protective effect of MCPs on I/R injury is related to neural stem cell (NSC) proliferation remains unclear. In the present study, we designed invivo and invitro experiments to elucidate the underlying mechanisms by which MCPs promote endogenous NSC proliferation during cerebral I/R. Invivo results showed that MCPs rescued the memory and learning abilities of rats after I/R damage and enhanced NSC proliferation in the rat subventricular zone (SVZ) and subgrannular zone (SGZ) during I/R. Invitro experiments demonstrated that MCPs could stimulate the proliferation of C17.2 cells under oxygen-glucose deprivation (OGD) conditions. Further studies revealed that the proliferation-promoting mechanism of MCPs relied on increasing the activity of SIRT1, decreasing the level of acetylation of β-catenin in the cytoplasm, and then triggering the translocation of β-catenin into the nucleus. These data provide experimental evidence that the up-regulation of SIRT1 activity by MCPs led to an increased cytoplasmic deacetylation of β-catenin, which promoted translocation of β-catenin to the nucleus to participate in the signaling pathway involved in NSC proliferation. The present study reveals that MCPs function as a therapeutic drug to promote stroke recovery by increasing the activity of SIRT1, decreasing the level of acetylated β-catenin, promoting the nuclear translocation of β-catenin and thereby increasing endogenous NSC proliferation.

Momordica charantia polysaccharides modulate the differentiation of neural stem cells via SIRT1/\u0392-catenin axis in cerebral ischemia/reperfusion

BackgroundStroke is the leading cause of long-term motor disability and cognitive impairment. Recently, neurogenesis has become an attractive strategy for the chronic recovery of stroke. It is important to understand the molecular mechanism that promotes neural stem cell (NSC) neurogenesis for future NSC-based therapies. Our previous study showed that Momordica charantia polysaccharides (MCPs) exerted neuroprotective effects on stroke via their anti-oxidant and anti-inflammation activities. However, it remains unknown whether MCPs promote NSC neurogenesis after cerebral ischemic/reperfusion injury (IRI).MethodsWe investigated MCPs’ function in differentiation of neural stem cells (NSCs) in vivo and in vitro experiments. Based on a middle cerebral artery occlusion (MCAO) rat model, the effect of MCPs on neuronal differentiation after MCAO was analyzed. Primary NSCs and neural stem cell line C17.2 were cultured and subjected to glutamate stimulation to establish the cell model of IRI. We evaluated the effect of MCPs on NSC differentiation in IRI cell model by Western blot and immunofluorescence staining. The SIRT1 activity of NSCs post glutamate stimulation was also evaluated by CELL SIRT1 COLORIMETRY ASSAY KIT. In addition, molecular mechanism was clarified by employing the activator and inhibitor of SIRT1.ResultsMCPs had no effects on the differentiation of neural stem cells under physiological conditions while shifted NSC differentiation potential from the gliogenic to neurogenic lineage under pathological conditions. Activation of SIRT1 with MCPs was responsible for the neuronal differentiation of C17.2-NSCs. The neuronal differentiation effect of MCPs was attributed to upregulation SIRT1-mediated deacetylation of β-catenin. MCP-induced deacetylation via SIRT1 promoted nuclear accumulation of β-catenin in NSCs.ConclusionOur findings indicate that the deacetylation of β-catenin by SIRT1 represents a critical mechanism of action of MCPs in promoting NSC neuronal differentiation. It provides an improved understanding of molecular mechanism underlying neuroprotective effects of MCPs in IRI, indicating its potential role on treating ischemic stroke especially chronic recovery.

Preparation, analysis, antioxidant activities in vivo of phosphorylated polysaccharide from Momordica charantia

Momordica charantia (bitter melon) is a kind of medicine and food homologous fruit. The Momordica charantia polysaccharide has the physiological functions of clearing away heat and detoxification, lowering blood sugar, improving immunity and so on. It is an ideal health care product. The extraction of Momordica charantia polysaccharide was carried out by hot water method. The structure of the polysaccharide and its phosphorylated derivative was determined by IR and NMR, which indicated that the chemical modification was successful. The polysaccharide could significantly increase the content of SOD and CAT in serum, liver and spleen tissue of mice, and reduce the content of MDA in serum, liver and spleen tissue to a certain extent.

Extraction and analysis of polysaccharide from Momordica charantia

Momordica charantia is a kind of medicine and food homologous fruit. The M. charantia polysaccharide has the physiological functions of clearing away heat and detoxification, lowering blood sugar, improving immunity and so on. It is an ideal health care product.MP3 from M. charantia polysaccharides were isolated and purified by DEAE cellulose column chromatography and gel column chromatography. The composition of polysaccharides was determined by thin layer chromatography (TLC) and gas chromatography, and the relative molecular weight was determined by gel filtration. The results showed there were typical absorption peaks of polysaccharide in its infrared spectrum, and there were no characteristic absorption peaks of nucleic acids and proteins in its ultraviolet scanning. MP3 contained rhamnose, xylose, galactose and arabinose, and its average molecular weight was 9.57 × 104. This method was easy to operate and laid a foundation for the development of M. charantia polysaccharide products.

Cold plasma treated phlorotannin/Momordica charantia polysaccharide nanofiber for active food packaging

Momordica charantia polysaccharide (MCP) has been repeatedly reported due to its anti-diabetic properties. Up to our knowledge, no research has discussed the use of MCP as a nanofiber matrix in an active food packaging. As an antibacterial and anti-oxidant agent, phlorotannin (PT) was encapsulated in MCP nanofibers to promote these activities. Nanofiber membranes were treated with cold plasma to increase their application performance. Antioxidant and antibacterial activities of PT and MCP against Escherichia coli O157:H7 were individually evaluated. The prepared nanofibers were assessed for their physical and mechanical properties in order to select the better-characterized ones. The successfulness of PT loading into MCP nanofibers was confirmed using SEM, AFM, TGA and DSC. After cold plasma treatment, the release efficiency of PT from the nanofibers was enhanced by 23.5 % (4 °C) and 25 % (25 °C), respectively. Correspondingly, both antibacterial and anti-oxidant activities of PT/MCP nanofibers were markedly improved.

Antioxidant activity of Momordica charantia polysaccharide and its derivatives

Momordica charantia polysaccharide (MCP) was extracted by hot water and chemically modified to obtain phosphorylated Momordica charantia polysaccharide (P-MCP) with degree of substitution 0.12 and sulfated Momordica charantia polysaccharide (S-MCP) with degree of substitution 0.45. The sugar content of the three polysaccharides was determined by phenol sulfuric acid method, 74.0%, 68.1% and 59.8% respectively. The scavenging ability of three polysaccharides to superoxide anion, hydroxyl radical and DPPH radical, as well as their anti-lipid peroxidation and reduction ability were determined. The results showed that the antioxidant activity of polysaccharides varied with different chemical modifications.

Behavioral defects induced by chronic social defeat stress are protected by Momordica charantia polysaccharides via attenuation of JNK3/PI3K/AKT neuroinflammatory pathway.

The aim of this study was to evaluate the protective effects of Momordica charantia polysaccharides (MCP) on depressive-like behaviors. The chronic social defeat stress (CSDS) mice model was used to evaluate the effects of MCP and their underlying mechanisms. Social interaction test (SIT), sucrose preference test (SPT), and tail suspension test (TST) were performed for behavioral assessments. Expression levels of inflammation mediators and phosphatidylinositol 3-kinase (PI3K) activity were determined using commercial ELISA kits. The expression of key proteins in the c-Jun N-terminal protein kinase (JNK3)/PI3K/protein kinase B (AKT) pathway were measured using western blot and RT-PCR. The results showed that chronic administration of MCP (100, 200, 400 mg/kg/day) significantly prevented depressive-like behaviors in CSDS mice as assessed by SIT, TST and SPT. Elevated levels of proinflammatory cytokines [tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β)], and expression of JNK3, c-Jun, P-110β proteins were observed in the hippocampus of CSDS mice. Moreover, the activity of PI3K and phosphorylation level of AKT were reduced in the hippocampus of CSDS mice. Interestingly, the administration of MCP reversed these changes. Furthermore, the protective effects of MCP on CSDS mice were partly inhibited by the PI3K inhibitor, LY294002. In conclusion, the protective effects of MCP against depressive-like behaviors in CSDS mice might be due to a reduction in neuroinflammation and the down-regulation of the JNK3/PI3K/AKT pathway in the hippocampus.

Polysaccharide from fermented Momordica charantia L. with Lactobacillus plantarum NCU116 ameliorates type 2 diabetes in rats

The influence of Lactobacillus plantarum-fermentation on the structure and anti-diabetic effects of Momordica charantia polysaccharides were evaluated. High-fat diet and streptozotocin-induced type 2 diabetic rats were administrated with polysaccharides from fermented and non-fermented Momordica charantia (FP and NFP) for 4 weeks. Fermentation affected the physicochemical characterization, monosaccharide composition, molecular weight, and viscosity of Momordica charantia polysaccharides. Treatment with FP significantly ameliorated hyperglycemia, hyperinsulinemia, hyperlipidemia, and oxidative stress in diabetic rats compared with NFP. Moreover, the diversity and abundance of gut microbiota (Lactococcus laudensis and Prevotella loescheii) in diabetic rats were notably increased by treatment with FP in comparison to NFP. Meanwhile, FP-treated diabetic rats exhibited more colonic short-chain fatty acids (SCFAs) and lower pH values than that in NFP-treated rats. Overall, Lactobacillus plantarum-fermentation could enhance the anti-diabetes effects of Momordica charantia polysaccharides in rats by modifying the structure of polysaccharides to optimize gut microbiota and heighten the production of SCFAs.

Transcriptomic analysis of Momordica charantia polysaccharide on streptozotocin-induced diabetic rats

Polysaccharides obtained from Momordica charantia have been shown to exert a hypoglycemic effect, thereby improving glucose metabolism. However, little is known regarding the molecular mechanisms underlying this process. In recent years, RNA sequencing (RNA-seq) has rapidly emerged as a major transcriptome profiling system. Herein, RNA-seq was utilized to obtain whole transcriptomes from the livers of SD rats with type 2 diabetes (DM) and type 2 diabetic rats treated with M. charantia polysaccharides (DMCPIIa). In total, 44,752,508–52,585,920 uniquely mapped reads were obtained, covering 85.54% of the annotated transcripts and representing 12,857 mRNA transcripts. Following analytical analysis, 17 differentially expressed genes (p < 0.05, false discovery rate q < 0.05) were identified in the DMCPIIa group relative to the DM group. Gene ontology and pathway analysis demonstrated that 17 differently expressed genes were enriched in specific biological processes mainly relating to glucose metabolism and fat metabolism (p < 0.05). Furthermore, a subset of the differential genes was selected for validation via real-time quantitative reverse-transcription PCR. Collectively, the integrated analysis of differential gene expression, data obtained herein and the examination of previously reported quantitative trait loci, and genome-wide association studies has suggested that pdk4, pkl, hsd11β1, msmo1, rbp4 and fads2 may serve as promising candidates for the modulation of type 2 diabetes.

Preparation of Bioactive Polysaccharide Nanoparticles with Enhanced Radical Scavenging Activity and Antimicrobial Activity.

Because of their biocompatibility and biodegradability in vivo, natural polysaccharides are effective nanocarriers for delivery of active ingredients or drugs. Moreover, bioactive polysaccharides, such as tea, Ganoderma lucidum, and Momordica charantia polysaccharides (TP, GLP, and MCP), have antibacterial, antioxidant, antitumor, and antiviral properties. In this study, tea, Ganoderma lucidum, and Momordica charantia polysaccharide nanoparticles (TP-NPs, GLP-NPs, and MCP-NPs) were prepared via the nanoprecipitation approach. When the ethanol to water ratio was 10:1, the diameter of the spherical polysaccharide nanoparticles was the smallest, and the mean particle size of the TP-NPs, GLP-NPs, and MCP-NPs was 99 ± 15, 95 ± 7, and 141 ± 9 nm, respectively. When exposed to heat, increased ionic strength and pH levels, the nanoparticles exhibited superior stability and higher activity than the corresponding polysaccharides. In physiological conditions (pH 7.4), the nanoparticles underwent different protein adsorption capacities in the following order: MCP-NPs> TP-NPs> GLP-NPs. Moreover, the 2,2-diphenyl-1-picrylhydrazyl (DPPH), hydroxyl radical, and superoxide anion radical scavenging rates of the nanoparticles were increased by 9-25% as compared to the corresponding polysaccharides. Compared to the bioactive polysaccharides, the nanoparticles enhanced antimicrobial efficacy markedly and exhibited long-acting antibacterial activity.

Momordica charantia polysaccharides ameliorate oxidative stress, inflammation, and apoptosis in ethanol-induced gastritis in mucosa through NF-kB signaling pathway inhibition

This study investigated the therapeutic role of polysaccharides from M. charantia and their mechanism of action against ethanol-induced gastric ulcers in rats. Their effects were determined through macroscopic evaluation of the gastric cavity (gastric ulcer index [GUI]), changes in PGE2, lipid peroxidation (malondialdehyde), antioxidant systems (catalase and reduced glutathione), inflammatory markers (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and myeloperoxidase [MPO]), apoptotic markers (caspase 3, Bax, and Bcl-2), nuclear factor-κB (NF-κB [p65]), and histopathological staining (H&E and PAS). Pretreatment with MCP (300mg/kg p.o.) attenuated the severity of ethanol-induced gastric mucosal damage, reductions in GUI, histopathologic aberrations, and neutrophil invasion, and PGE2 upregulation. These actions were similar to those of omeprazole, a reference anti-ulcer drug. MCP repressed gastric inflammation through the reduction of MPO, TNF-α, and IL-6, and prevented gastric oxidative stress through the inhibition of lipid peroxides with the concomitant enhancement of glutathione and catalase activity. Apoptotic markers indicated that MCP suppressed Bax and caspase-3 activity and enhanced the anti-apoptotic protein Bcl-2, which favored cell survival. MCP downregulated NF-κB and upregulated IκBα. Our study results suggested that the prophylactic administration of MCP reduced ethanol-induced gastric injury in rats through the suppression of gastric inflammation and oxidative stress, predominantly via NF-κB inhibition.

Analysis of &amp;lt;i&amp;gt;Momordica charantia&amp;lt;/i&amp;gt; Polysaccharide Components and Their Effects on KA-Induced Oxidative Stress and Neuronal Loss in the Hippocampus of Epileptic Rats

Polysaccharides of Momordica charantia have been reported to be the primary bioactive components that confer its antioxidant activity. To some degree, antioxidants may provide beneficial effects on neuronal damage induced by seizures. However, the protective effects of Momordica charantia polysaccharides (MCPs) on seizures remain unclear. In this study, our purpose was to investigate the effects of MCPs on oxidative stress and neurodegeneration in an experimental Kainic acid (KA)-induced rat seizure model. MCPs treatments decreased the level of malondialdehyde (MDA) and increased the activities of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus of the KA-induced animal model. Moreover, MCPs significantly attenuated KA-induced neuronal loss in the CA1 and CA3 hippocampal regions. Based on these results, MCPs exert neuroprotective effects by attenuating KA-induced neuronal damage in the brain through their free radical scavenging activities.

Effects of Momordica charantia polysaccharide on in vitro ruminal fermentation and cellulolytic bacteria

Four levels of Momordica charantia polysaccharide (MCP) supplements (0, 0.1, 0.3, 0.6 mg/ml) were designed to investigate the effects of MCP on ruminal fermentation and cellulolytic bacteria in vitro. The pH, ammonia-N (NH3-N) and volatile fatty acids (VFA) were measured at 6, 24, 48 h, whilst the cellulolytic bacteria population was determined at 6 and 24 h. The 0.6 mg/ml MCP inclusion decreased the theoretical maximum of gas production and the half-life. The NH3-N concentration was decreased by MCP at all doses at 24 h. The MCP inclusion increased the concentration of total VFA at 24 and 48 h and the acetate to propionate ratio, the molar proportion of isovalerate at 6 h, while decreased that of isobutyrate at 24 h and that of isovalerate, valerate at 24 and 48 h, respectively. The relative abundances of Ruminococcus albus and Ruminococcus flavefaciens were decreased at 6 h, while that of Butyrivibrio fibrisolvens was increased at all times of incubation and that of Fibrobacter succinogenes reached the greatest value at 0.6 mg/ml MCP supplementation at 24 h. This study demonstrated that the MCP had the ability to enhance the total VFA production, modulate the rumen fermentation pathway and influence the number of cellulolytic bacteria population.