The association between hepatitis C virus infection status and blood pressure in adults in the United States: NHANES 1999-2012.

Background: The Hepatitis C virus (HCV) infection is strongly associated with cardiovascular disease risk factors, but the relationship with blood pressure (BP) remains unclear. Objectives: To assess the association between HCV infection status and BP in US adults. Methods: Data for the study were obtained from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2012. The association of HCV infection status (including HCV infection, current HCV infection, and past HCV infection) with hypertension, systolic blood pressure (SBP), and diastolic blood pressure (DBP) were explored using logistic or linear regression analyses respectively. Results: A total of 25,850 participants (age≥18 years) were enrolled in the current study, including 14,162 participants with hypertension. After adjusting for all covariates, HCV infection/current HCV infection was not associated with hypertension and SBP compared to participants with non-HCV infection (OR: 1.34,95% CI 0.96-1.87/1.31 95% CI 0.91,1.91, ß: -0.92, 95% CI -2.7-0.86/-0.35 95% CI -2.51,1.81, respectively). HCV infection/current HCV infection was only associated with elevated DBP (ß: 4.1,95% CI 2.57-5.63/4.24,95% CI 2.27-6.21). However, there was no correlation with past HCV infection in participants with hypertension, SBP, and DBP compared to those with non-HCV infection (OR: 1.23,95% CI 0.59-2.54; ß: -3.79, 95% CI -7.67-0.08 and 2.28 95% CI -0.36-4.92, respectively). Conclusion: In a representative sample of US adults, it was found that both HCV infection and current HCV infection were independently linked to higher DBP. However, there was no association between past HCV infection and DBP.

Ganoderic acid A mitigates dopaminergic neuron ferroptosis via inhibiting NCOA4-mediated ferritinophagy in Parkinson's disease mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Ganoderma lucidum, a renowned tonic traditional Chinese medicine, is widely recognized for the exceptional activity in soothing nerves and nourishing the brain. It has been extensively employed to alleviate various neurological disorders, notably Parkinson's disease (PD). AIM OF THE STUDY: To appraise the antiparkinsonian effect of GAA, the main bioactive constituent of G. lucidum, and clarify the molecular mechanism through the perspective of ferritinophagy-mediated dopaminergic neuron ferroptosis. MATERIALS AND METHODS: PD mouse and cell models were established using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (MPP+), respectively. Cell viability, behavioral tests and immunofluorescence analysis were performed to evaluate the neurotoxicity, motor dysfunction and dopaminergic loss, respectively. Biochemical assay kits were used to determine the levels of iron, lipid reactive oxygen species (ROS), malondialdehyde (MDA), total ROS and glutathione (GSH). Western blot and immunofluorescence were applied to detect the expressions of nuclear receptor co-activator 4 (NCOA4), ferritin heavy chain 1 (FTH1), p62 and LC3B. Additionally, NCOA4-overexpressing plasmid vector was constructed to verify the inhibitory effect of GAA on the neurotoxicity and ferroptosis-related parameters in PD models. RESULTS: GAA significantly mitigated MPP+/MPTP-induced neurotoxicity, motor dysfunction and dopaminergic neuron loss (p＜0.01 or p＜0.05). In contrast to MPP+/MPTP treatment, GAA treatment decreased the levels of iron, MDA, lipid and total ROS, while increasing the GSH level. GAA also reduced the levels of NCOA4 and LC3B, and enhanced the expressions of FTH1 and p62 in PD models (p＜0.01 or p＜0.05). However, the protective effect of GAA against the neurotoxicity, NCOA4-mediated ferritinophagy and ferroptosis in PD model was abolished by the overexpression of NCOA4 (p＜0.01). CONCLUSION: GAA exerted a protective effect on PD, and this effect was achieved by suppressing dopaminergic neuron ferroptosis through the inhibition of NCOA4-mediated ferritinophagy.

Tea Polysaccharide Ameliorates High-Fat Diet-Induced Renal Tubular Ectopic Lipid Deposition via Regulating the Dynamic Balance of Lipogenesis and Lipolysis.

Renal tubular ectopic lipid deposition (ELD) plays a significant role in the development of chronic kidney disease, posing a great threat to human health. The present work aimed to explore the intervention effect and potential molecular mechanism of a purified tea polysaccharide (TPS3A) on renal tubular ELD. The results demonstrated that TPS3A effectively improved kidney function and slowed the progression of tubulointerstitial fibrosis in high-fat-diet (HFD)-exposed ApoE-/- mice. Additionally, TPS3A notably suppressed lipogenesis and enhanced lipolysis, as shown by the downregulation of lipogenesis markers (SREBP-1 and FAS) and the upregulation of lipolysis markers (HSL and ATGL), thereby reducing renal tubular ELD in HFD-fed ApoE-/- mice and palmitic-acid-stimulated HK-2 cells. The AMPK-SIRT1-FoxO1 axis is a core signal pathway in regulating lipid deposition. Consistently, TPS3A significantly increased the levels of phosphorylated-AMPK, SIRT1, and deacetylation of Ac-FoxO1. However, these effects of TPS3A on lipogenesis and lipolysis were abolished by AMPK siRNA, SIRT1 siRNA, and FoxO1 inhibitor, resulting in exacerbated lipid deposition. Taken together, TPS3A shows promise in ameliorating renal tubular ELD by inhibiting lipogenesis and promoting lipolysis through the AMPK-SIRT1-FoxO1 signaling pathway.

High serum copper as a risk factor of all-cause and cause-specific mortality among US adults, NHANES 2011-2014.

Background: Several studies have shown that serum copper levels are related to coronary heart disease, diabetes, and cancer. However, the association of serum copper levels with all-cause, cause-specific [including cardiovascular disease (CVD) and cancer] mortality remains unclear. Objectives: This study aimed to prospectively examine the association of copper exposure with all-cause, CVD, and cancer mortality among US adults. Methods: The data for this analysis was obtained from the National Health and Nutrition Examination Survey (NHANES) between 2011 and 2014. Mortality from all-causes, CVD, and cancer mortality was linked to US National Death Index mortality data. Cox regression models were used to estimate the association between serum copper levels and all-cause, CVD, and cancer mortality. Results: A total of 2,863 adults were included in the main study. During the mean follow-up time of 81.2 months, 236 deaths were documented, including 68 deaths from cardiovascular disease and 57 deaths from cancer. The weighted mean overall serum copper levels was 117.2 ug/L. After adjusting for all of the covariates, compared with participants with low (1st tertile, <103 µg/L)/medium (2st tertile, 103-124 µg/L) serum copper levels, participants with high serum copper levels (3rd tertile, ≥124 µg/L) had a 1.75-fold (95% CI, 1.05-2.92)/1.78-fold (1.19,2.69) increase in all-cause mortality, a 2.35-fold (95% CI, 1.04-5.31)/3.84-fold (2.09,7.05) increase in CVD mortality and a 0.97-fold (95% CI, 0.28-3.29)/0.86-fold (0.34,2.13) increase in cancer mortality. In addition, there was a linear dose-response association between serum copper concentration with all-cause and CVD mortality (P for nonlinear > 0.05). Conclusions: This prospective study found that serum copper concentrations were linearly associated with all-cause and CVD mortality in US adults. High serum copper levels is a risk factor for all-cause and CVD mortality.

Halting Multiple Myeloma with MALT1 Inhibition: Suppressing BCMA-Induced NF-κB and Inducing Immunogenic Cell Death.

As multiple myeloma (MM) poses a formidable therapeutic challenge despite recent progress, exploring novel targets is crucial. Mucosa-associated lymphoid tissue lymphoma translocation protein-1 (MALT1) emerges as a promising paracaspase with druggable potential, especially unexplored in MM. Our study provided compelling evidence demonstrating a statistically significant elevation of MALT1 expression in human primary MM cells. Moreover, elevated MALT1 expression was associated with a poorer prognosis in MM. Genetic deletion of MALT1 reduced cell growth, colony formation, and tumor growth in vivo. Pharmacological inhibition with 1 µM Mi-2 effectively inhibited cell growth, inducing mitochondria-dependent apoptotic cell death. Mechanistically, MALT1 inhibition disrupted diverse signal transduction pathways, notably impeding nuclear factor κB (NF-κB). Significantly, the inhibition of MALT1 demonstrated a substantial suppression of NF-κB activation by elevating IκB, disrupting the nuclear localization of p65 and c-Rel. This effect was observed in both the basal state and when stimulated by BCMA, highlighting the pivotal role of MALT1 inhibition in influencing MM cell survival. It was noteworthy that Mi-2 induces properties associated with immunogenic cell death (ICD), as evidenced by increased calreticulin (CRT), ATP release, and high-mobility group protein B1 (HMGB1) upregulation, consequently triggering ICD-associated immune activation and enhancing CD8+ T - cell cytotoxicity in vitro. In conclusion, our research highlights MALT1 as a promising druggable target for therapeutic interventions in MM, providing insights into its molecular mechanisms in MM progression.

Rapid Discovery of Aß42 Fibril Disintegrators from Ganoderma lucidum via Ligand Fishing and Their Neuroprotective Effects on Alzheimer's Disease.

An amyloid-ß (Aß) fibril is a vital pathogenic factor of Alzheimer's disease (AD). Aß fibril disintegrators possess great potential to be developed into novel anti-AD agents. Here, a ligand fishing method was employed to rapidly discover Aß42 fibril disintegrators from Ganoderma lucidum using Aß42 fibril-immobilized magnetic beads, which led to the isolation of six Aß42 fibril disintegrators including ganodermanontriol, ganoderic acid DM, ganoderiol F, ganoderol B, ganodermenonol, and ergosterol. Neuroprotective evaluation in vitro exhibited that these Aß42 fibril disintegrators could significantly mitigate Aß42-induced neurotoxicity. Among these six disintegrators, ergosterol and ganoderic acid DM with stronger protecting activity were further selected to evaluate their neuroprotective effect on AD in vivo. Results showed that ergosterol and ganoderic acid DM could significantly alleviate Aß42-induced cognitive dysfunction and hippocampus neuron loss in vivo. Moreover, ergosterol and ganoderic acid DM could significantly inhibit Aß42-induced neuron apoptosis and Nrf2-mediated neuron oxidative stress in vitro and in vivo.

Impact of cellulose and lignin on restoration of vegetation and soil chemical properties for saline-alkali soil of songnen plain.

To explore the effects of cellulose and lignin on stimulating vegetation restoration and improving soil chemical properties in saline-alkali soil, a large area test was carried out, and 2 treatments were set up: T (cellulose and lignin+ Planted seeds) and CK (Planted seeds). In this study, the species, quantity, plant height, above-ground biomass, biodiversity of vegetation in the treated plots, the determination of soil chemical nutrient content, and the effect of cellulose and lignin on vegetation restoration in saline-alkali land were investigated. The results showed that: 1) Cellulose and lignin contributed to vegetation growth. Compared with CK treatment, plant height and aboveground biomass of T increased by 158.73% and 240.13%, respectively; 2) Cellulose and lignin improved soil structure, and soil porosity, and decreased soil compaction (21.95%); 3) Compared with CK treatment, T treatment decreased soil pH by 0.5 units, total salt content decreased by 30.95%, exchangeable Na+ decreased by 63.00%, and exchangeable sodium percentage (ESP) decreased by 61.51%. Furthermore, cellulose and lignin effectively improved the physical and chemical properties of saline-alkali soil, promoted the recovery of ecological environment in saline-alkali soil, and improved regional biodiversity, which will provide new methods for soil remediation and improvement in saline-alkali areas.

Codonopsis lanceolata polysaccharide ameliorates high-fat diet induced-postpartum hypogalactia via stimulating prolactin receptor-mediated Jak2/Stat5 signaling.

This study aims to investigate the ameliorative effect of Codonopsis lanceolata polysaccharide (PCL) on mice with hypogalatia induced by a high-fat diet (HFD) and the potential underlying mechanism. We found that oral administration of PCL demonstrated significant benefits in countering the negative effects of HFD, including weight gain, hepatic steatosis, mesenteric adipocyte hypertrophy, and abnormal glucose/lipid metabolism. In addition, PCL improved mammary gland development and enhanced lactogenesis performance. Histologically, PCL ameliorated the retardation of ductal growth, reduced mammary fat pad thickness, improved the incomplete linear encapsulation of luminal epithelium and myoepithelium, and increased the proliferation of mammary epithelial cells. Flow cytometry analysis showed that PCL mitigated the detrimental effects of HFD on mammary gland development by promoting the proliferation and differentiation of mammary epithelial cells. Mechanistic studies revealed that PCL upregulated the levels of prolactin (PRL) and its receptor (PRLR) in the mammary gland, activated JAK2/STAT5 signaling pathway, and increased the expression of p63, ERBB4, and NRG1. Overall, PCL can ameliorate HFD-induced hypogalactia by activating PRLR-mediated JAK2/STAT5 signaling. Our findings offer a methodological and theoretical foundation for investigating the functional constituents of traditional Chinese medicine in the treatment of hypogalactia.

Purification, structural characteristics and anti-atherosclerosis activity of a novel green tea polysaccharide.

A new homogeneous polysaccharide (TPS3A) was isolated and purified from Tianzhu Xianyue fried green tea by DEAE-52 cellulose and Sephacryl S-500 column chromatography. Structural characterization indicated that TPS3A mainly consisted of arabinose, galactose, galacturonic acid and rhamnose in a molar ratio of 5.84: 4.15: 2.06: 1, with an average molecular weight of 1.596 × 104 kDa. The structure of TPS3A was characterized as a repeating unit consisting of 1,3-Galp, 1,4-Galp, 1,3,6-Galp, 1,3-Araf, 1,5-Araf, 1,2,4-Rhap and 1-GalpA, with two branches on the C6 of 1,3,6-Galp and C2 of 1,2,4-Rhap, respectively. To investigate the preventive effects of TPS3A on atherosclerosis, TPS3A was administered orally to ApoE-deficient (ApoE-/-) mice. Results revealed that TPS3A intervention could effectively delay the atherosclerotic plaque progression, modulate dyslipidemia, and reduce the transformation of vascular smooth muscle cells (VSMCs) from contractile phenotype to synthetic phenotype by activating the expression of contractile marker alpha-smooth muscle actin (α-SMA) and inhibiting the expression of synthetic marker osteopontin (OPN) in high-fat diet-induced ApoE-/- mice. Our findings suggested that TPS3A markedly alleviated atherosclerosis by regulating dyslipidemia and phenotypic transition of VSMCs, and might be used as a novel functional ingredient to promote cardiovascular health.

Prevalence of Chronic Kidney Disease Among US Adults With Hypertension, 1999 to 2018.

BACKGROUND: Hypertension is a major cause of end-stage renal disease. Assessing temporal trends in the prevalence of chronic kidney disease (CKD) in hypertension could provide information for public health policies and plans. METHODS: From the National Health and Nutrition Examination Survey from 1999 to 2018, a probability sample of adults aged ≥20 years was collected. The primary outcomes were classified according to the estimated glomerular filtration rate and urinary albumin. Trend tests were performed to assess age-standardized prevalence trends of CKD, albuminuria, and macroalbuminuria in US adults with hypertension. RESULTS: A total of 23 120 US adults with hypertension were included in this study. The prevalence of any CKD, albuminuria, or macroalbuminuria in hypertension remained relatively stable. However, the age-standardized prevalence of stage 1 CKD in hypertension increased from 4.9% in 2003 to 2006 to 7.0% in 2015 to 2018 (P=0.0077 for trend). The age-standardized prevalence of stage 3b CKD in hypertension decreased from 2.9% in 2011 to 2014 to 2.1% in 2015 to 2018 (P=0.0350 for trend). A similar trend was observed for the age-standardized prevalence of stages 3 to 5 CKD in hypertension, which declined from 10.9% in 2011 to 2014 to 8.9% in 2015 to 2018 (P=0.0160 for trend). CONCLUSIONS: Among US adults with hypertension, the prevalence of any CKD, albuminuria, and macroalbuminuria remained relatively stable from 1999 to 2018, whereas the hypertensive population showed an increasing trend in stage 1 CKD from 2003 to 2006 to 2015 to 2018 and a decreasing trend in the prevalence of stages 3 to 5 and 3b CKD from 2011 to 2014 to 2015 to 2018.

The STAT3 inhibitor stattic overcome bortezomib-resistance in multiple myeloma via decreasing PSMB6.

Bortezomib, an FDA approved drug in 2003 for newly diagnosed and relapsed/refractory MM, had showed great efficacy in different clinical settings. However, many patients still developed resistance to Bortezomib, and the mechanism of action remains unelucidated. Here, we showed that Bortezomib resistance can be partially overcome by targeting a different subunit of 20 S complex - PSMB6. PSMB6 knock down by shRNA increased sensitivity to Bortezomib in resistant and sensitive cell line. Interestingly, a STAT3 inhibitor, Stattic, is shown to selectively inhibit PSMB6 and induce apoptosis in Bortezomib resistant and sensitive MM cells, even with IL-6 induction. Therefore, PSMB6 is a novel target for Bortezomib resistance and Stattic may offer a potential therapeutic strategy.

Laminaria japonica polysaccharide attenuates podocyte epithelial-mesenchymal transformation via TGF-ß1-mediated Smad3 and p38MAPK pathways.

In the present work, we explored the interventional effect and potential mechanism of a purified Laminaria japonica polysaccharide (LJP61A) on podocyte epithelial-mesenchymal transition (EMT) in TGF-ß1-induced podocytes and adriamycin-treated mice. Results showed that compared to the model groups, LJP61A significantly up-regulated the levels of epithelial markers (Nephrin, WT-1, podocin) and down-regulated the levels of mesenchymal markers (α-SMA, FN1) in vitro and in vivo, thus preventing EMT-like morphological changes of podocytes, proteinuria and kidney injury. Smad3 and p38MAPK are two central pathways mediating podocyte EMT activated by TGF-ß1. We found that LJP61A suppressed TGF-ß1-induced activation of Smad3, Smad4 and p38MAPK in vitro and in vivo. Moreover, the inhibitory actions of LJP61A on podocyte EMT were synergistically strengthened by Smad3 inhibitor SIS3 and p38MAPK inhibitor SB203580. Taken together, these findings revealed that LJP61A could prevent podocyte EMT, which might be related to the inhibition of TGF-ß1-mediated Smad3 and p38MAPK pathways.

Inhibition of Ca2+-calpain signaling is a new mechanism using Laminaria japonica polysaccharide to prevent macrophage foam cell formation and atherosclerosis.

The Ca2+-calpain signaling plays a pivotal role in regulating the upstream signaling pathway of cellular autophagy. The aim of the current work was to investigate the role of Ca2+-calpain signaling in the regulation of macrophage autophagy by a Laminaria japonica polysaccharide (LJP61A) in Ox-LDL induced macrophages and high fat diet fed atherosclerotic mice. Results revealed that the LJP61A markedly decreased the levels of intracellular Ca2+, calpain1, calpain2 and their downstream effectors (Gsα, cAMP and IP3), and simultaneously enhanced autophagy activity and lipid metabolism, thereby reducing lipid accumulation in the Ox-LDL stimulated macrophages and lipid-laden plaques in atherosclerotic mice. Moreover, BAPTA-AM (a Ca2+ chelator) and calpeptin (a calpain inhibitor) synergistically strengthened the beneficial effects of LJP61A on autophagy and lipid metabolism by decreasing the levels of intracellular Ca2+, calpain1, calpain2, and their downstream effectors (Gsα, cAMP and IP3) induced by Ox-LDL. These findings suggested that the LJP61A suppressed macrophage derived foam cell formation and atherosclerosis by modulating the Ca2+-calpain-mediated autophagy.

Polygonatum cyrtonema Hua Polysaccharide Alleviates Fatigue by Modulating Osteocalcin-Mediated Crosstalk between Bones and Muscles.

Osteocalcin was reported to regulate muscle energy metabolism, thus fighting fatigue during exercise. The current work aimed to investigate the anti-fatigue effect and the underlying mechanism of a homogeneous polysaccharide (PCPY-1) from Polgonatum cyrtonema after structure characterization. In the exhaustive swimming mouse model and the co-culture system of BMSCs/C2C12 cells, PCPY-1 significantly stimulated BMSC differentiation into osteoblasts as determined by ALP activity, matrix mineralization, and the protein expressions of osteogenic markers BMP-2, phosphor-Smad1, RUNX2, and osteocalcin. Meanwhile, PCPY-1 remarkably enhanced myoblast energy metabolism by upregulating osteocalcin release and GPRC6A protein expression; the phosphorylation levels of CREB and HSL; the mRNA levels of GLUT4, CD36, FATP1, and CPT1B; and ATP production in vitro and in vivo. Accordingly, PCPY-1 exhibited good anti-fatigue capacity in mice as confirmed by fatigue-related indicators. Our findings indicated PCPY-1 could enhance osteocalcin-mediated communication between bones and muscles, which was conducive to muscle energy metabolism and ATP generation, thus alleviating fatigue in exhausted swimming mice.

Dendrobium huoshanense stem polysaccharide ameliorates alcohol-induced gastric ulcer in rats through Nrf2-mediated strengthening of gastric mucosal barrier.

This study aimed to explore whether Dendrobium huoshanense stem polysaccharide (cDHPS) ameliorates alcohol-induced gastric ulcer (GU) through the strengthening effect of the gastric mucosal barrier in rats and its potential mechanism. In normal rats, the pretreatment of cDHPS effectively strengthened gastric mucosal barrier by increasing mucus secretion and tight junction protein expression. In GU rats, cDHPS supplementation effectively alleviated alcohol-induced gastric mucosal injury and nuclear factor κB (NF-κB)-driven inflammation by strengthening gastric mucosal barrier. Moreover, cDHPS significantly activated nuclear factor E2-related factor 2 (Nrf2) signaling and promoted antioxidant enzymes activities in both normal and GU rats. These results suggested that the pretreatment of cDHPS could strengthen gastric mucosal barrier to inhibit oxidative stress and NF-κB-driven inflammation induced gastric mucosal injury, which was likely related to the activation of Nrf2 signaling.

Dendrobium fimbriatum polysaccharide ameliorates DSS-induced intestinal mucosal injury by IL-22-regulated intestinal stem cell regeneration.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease with unknown etiology and difficult treatment. In this study, the intervention effect of Dendrobium fimbriatum Hook polysaccharide (cDFPW1) on UC was verified by constructing a dextran sulfate sodium (DSS)-induced colitis mouse model, and the protective effect of cDFPW1 on intestinal mucosal integrity in UC was explored by the co-culture system consisting of intestinal organoids and lamina propria lymphocytes (LPLs) combined with the experiment of microbial depletion mice. Results showed that cDFPW1 significantly alleviated UC symptoms in mice and promoted the proliferation of intestinal epithelial cells. Importantly, cDFPW1 could directly improve DSS-induced morphological damage of intestinal organoids and increase the number of epithelial cells, which was validated in mice. During repair, an increase in the number of Lgr5+ cells in intestinal organoids and mouse intestines was promoted by cDFPW1. Meanwhile, cDFPW1 promoted intestinal stem cells (ISCs)-mediated intestinal epithelial regeneration by significantly upregulating IL-22 expression. We further confirmed that the secretion of IL-22 was mediated by LPLs. Together, these findings suggest that cDFPW1 promotes ISCs regeneration by LPLs-mediated up-regulation of IL-22 to protect the intestinal mucosal integrity, thereby playing an important role in improving UC.

Choose Appropriate Subproblems for Collaborative Modeling in Expensive Multiobjective Optimization.

In dealing with the expensive multiobjective optimization problem, some algorithms convert it into a number of single-objective subproblems for optimization. At each iteration, these algorithms conduct surrogate-assisted optimization on one or multiple subproblems. However, these subproblems may be unnecessary or resolved. Operating on such subproblems can cause server inefficiencies, especially in the case of expensive optimization. To overcome this shortcoming, we propose an adaptive subproblem selection (ASS) strategy to identify the most promising subproblems for further modeling. To better leverage the cross information between the subproblems, we use the collaborative multioutput Gaussian process surrogate to model them jointly. Moreover, the commonly used acquisition functions (also known as infill criteria) are investigated in this article. Our analysis reveals that these acquisition functions may cause severe imbalances between exploitation and exploration in multiobjective optimization scenarios. Consequently, we develop a new acquisition function, namely, adaptive lower confidence bound (ALCB), to cope with it. The experimental results on three different sets of benchmark problems indicate that our proposed algorithm is competitive. Beyond that, we also quantitatively validate the effectiveness of the ASS strategy, the CoMOGP model, and the ALCB acquisition function.

Hydrolytic Quinoa Protein and Cationic Lotus Root Starch-Based Micelles for Co-Delivery of Quercetin and Epigallo-catechin 3-Gallate in Ulcerative Colitis Treatment.

The accumulation and sustained release of drugs in the colonic inflammatory region are the favorable strategy for treating ulcerative colitis (UC). In this study, we developed a synergistic anti-inflammatory drug (quercetin/EGCG)-loaded micelle using hydrolytic quinoa protein (HQP) and cationic lotus root starch (CLRS) by a layer-by-layer assembly method. The encapsulation efficiency of quercetin and EGCG in the Que-HQP-EGCG-CLRS micelles reached 91.5 and 89.4%, respectively. This composite micelle exhibited a core-shell structure, where Que-HQP-EGCG was the core and CLRS was the coating shell. Moreover, the in vitro experiments indicated that these micelles can make Que/EGCG pass through gastric environments stably and delay their release in the intestine. Animal experiments further confirmed that the Que-HQP-EGCG-CLRS micelles can efficiently accumulate in the colonic inflammatory region and enable sustained release of drugs (more than 24 h), thus notably alleviating the symptoms of UC. These results suggested that Que-HQP-EGCG-CLRS micelles have good gastric stability, colonic inflammatory-accumulated effect, and sustained drug release ability, which are a promising co-delivery system for UC treatment.

Bioactive polysaccharides and their potential health benefits in reducing the risks of atherosclerosis: A review.

Atherosclerosis is a kind of lipid-driven chronic inflammatory disease of arteries and is the principal pathological basis of life-threatening cardiovascular disease events, such as strokes and heart attacks. Clinically, statins are the most commonly prescribed drugs for the treatment of atherosclerosis, but prolonged use of these drugs exhibit many adverse reactions and have limited efficacy. Polysaccharides are important natural biomacromolecules widely existing in plants, animals, microorganisms and algae. They have drawn considerable attention worldwide due to their multiple healthy functions, along with their non-toxic property. Importantly, a growing number of studies have demonstrated that bioactive polysaccharides exhibit prominent efficiency in controlling atherosclerotic risk factors like hyperlipemia, hypertension, oxidative stress, and inflammation. In recent decades, various bioactive polysaccharides with different structural features and anti-atherosclerotic potential from natural sources have been isolated, purified, and characterized. The aim of this review is to focus on the research progress of natural polysaccharides in reducing the risks of atherosclerosis based on evidence of in vitro and in vivo studies from 1966 to 2022. PRACTICAL APPLICATIONS: In the future, it is still necessary to strengthen the research on the development and mechanism of polysaccharides with anti-atherosclerotic potential. These anti-atherosclerotic polysaccharides with different structural characteristics and physiochemical properties from different sources will constitute a huge source of materials for future applications, especially in functional foods and drugs. The information summarized here may serve as useful reference materials for further investigation, production, and application of these polysaccharides in functional foods and therapeutic agents.