Ginkgo biloba extract (EGb-761) confers neuroprotection against ischemic stroke by augmenting autophagic/lysosomal signaling pathway.

Ginkgo biloba extract (EGb-761) is well-recognized to have neuroprotective properties. Meanwhile, autophagy machinery is extensively involved in the pathophysiological processes of ischemic stroke. The EGb-761 is widely used in the clinical treatment of stroke patients. However, its neuroprotective mechanisms against ischemic stroke are still not fully understood. The present study was conducted to uncover whether the pharmacological effects of EGb-761 can be executed by modulation of the autophagic/lysosomal signaling axis. A Sprague-Dawley rat model of ischemic stroke was established by middle cerebral artery occlusion (MCAO) for 90 min, followed by reperfusion. The EGb-761 was then administered to the MCAO rats once daily for a total of 7 days. Thereafter, the penumbral tissues were acquired to detect proteins involved in the autophagic/lysosomal pathway including Beclin1, LC-3, SQSTM1/p62, ubiquitin, cathepsin B, and cathepsin D by western blot and immunofluorescence, respectively. Subsequently, the therapeutic outcomes were evaluated by measuring the infarct volume, neurological deficits, and neuron survival. The results showed that the autophagic activities of Beclin1 and LC3-II in neurons were markedly promoted by 7 days of EGb-761 therapy. Meanwhile, the autophagic cargoes of insoluble p62 and ubiquitinated proteins were effectively degraded by EGb-761-augmented lysosomal activity of cathepsin B and cathepsin D. Moreover, the infarction size, neurological deficiencies, and neuron death were also substantially attenuated by EGb-761 therapy. Taken together, our study suggests that EGb-761 exerts a neuroprotective effect against ischemic stroke by promoting autophagic/lysosomal signaling in neurons at the penumbra. Thus, it might be a new therapeutic target for treating ischemic stroke.

Electrostatic assembly of gold nanoparticle and metal-organic framework nanoparticles attenuates amyloid ß aggregate-mediated neurotoxicity.

The deposition of amyloid ß (Aß) is a conventional pathological hallmark of Alzheimer's disease (AD). Consequently, the inhibition of Aß aggregation combined with the disaggregation of Aß fibrils is an important therapeutic method for AD treatment. In this study, a gold nanoparticle-decorated porous metal organic framework MIL-101(Fe) (AuNPs@PEG@MIL-101) was created as an Aß inhibitor. The high positively charged MIL-101 induced a high number of Aß40 to be absorbed or aggregated on the surface of nanoparticles. In addition, AuNPs improved the surface property of MIL-101, causing it to uniformly bind Aß monomers and Aß fibrils. Thus, this framework can efficiently suppress extracellular Aß monomer fibrillation and disrupt the preformed Aß fibers. AuNPs@PEG@MIL-101 also decreases intracellular Aß40 aggregation and the amount of Aß40 immobilized on the cell membrane, thus protecting PC12 cells from Aß40-induced microtubular defects and cell membrane damage. In summary, AuNPs@PEG@MIL-101 shows great potential for application in AD therapy.

Resveratrol-loaded selenium/chitosan nano-flowers alleviate glucolipid metabolism disorder-associated cognitive impairment in Alzheimer's disease.

Resveratrol (Res) is a common natural polyphenol that inhibits inflammation and oxidative stress in Alzheimer's disease (AD). However, the absorption efficiency and in vivo bioactivity of Res are poor. High fat diet-induced metabolic disorders, including obesity and insulin resistance, can promote AD-related ß-amyloid (Aß) aggregation, Tau protein phosphorylation and neurotoxicity. Gut microbiota play a role in modulating metabolic syndrome and cognitive impairment. Herein, flower-like Res-loaded selenium nanoparticles/chitosan nanoparticles (Res@SeNPs@Res-CS-NPs) with higher loading capacity (64 %) were prepared to regulate gut microbiota in cases of AD with metabolic disorder. The nano-flowers could restore gut microbiota homeostasis to reduce lipopolysaccharide (LPS) formation and LPS-induced neuroinflammation. Additionally, Res@SeNPs@Res-CS-NPs can prevent lipid deposition and insulin resistance by decreasing Firmicutes levels and increasing Bacteroidetes levels in the gut, further inhibiting Aß aggregation and Tau protein phosphorylation through the JNK/AKT/GSK3ß signaling pathway. Moreover, Res@SeNPs@Res-CS-NPs treatment was able to regulate the relative levels of gut microbiota associated with oxidative stress, inflammation and lipid deposition, including Entercoccus, Colidextribacter, Rikenella, Ruminococcus, Candidatus_Saccharimonas, Alloprevotella and Lachnospiraceae_UCG-006. Overall, Res@SeNPs@Res-CS-NPs significantly enhances cognitive ability in AD mice with metabolic disorder, highlighting their potential for preventing cognitive impairments in AD.

Brain targeted peptide-functionalized chitosan nanoparticles for resveratrol delivery: Impact on insulin resistance and gut microbiota in obesity-related Alzheimer's disease.

The pathology of Alzheimer's disease (AD) is highly correlated with obesity-induced insulin resistance. Resveratrol (Res) is a natural phenol that demonstrates a neuroprotective effect, but the bioactivity of Res is low in vivo. Here, chitosan (CS) was cross-linked with sodium tripolyphosphate (TPP) to encapsulate low water solubility Res. Next, a brain-targeted peptide (TG: TGNYKALHPHNG) was modified on the surface of Res-loaded CS/TPP nanoparticles (TG-Res-CS/TPP-NPs) to specifically deliver Res to the brain. Morris water maze results indicated that cognitive impairments were ameliorated by TG-Res-CS/TPP-NPs in obesity-related AD mice. Obesity-related insulin resistance promotes Tau phosphorylation and Aß aggregation in the brain. Administration of TG-Res-CS/TPP-NPs alleviated lipid deposition-induced insulin resistance and decreased the level of phosphorylated Tau and Aß aggregation via the JNK/AKT/GSK3ß pathway. Additionally, TG-Res-CS/TPP-NPs transported across blood-brain barrier which in turn increased glucose transporter expression levels, antioxidant enzyme activity and inhibited microglial cell activation. Thus, TG-Res-CS/TPP-NPs were more effective than Res-CS/TPP-NPs at regulating glucose homeostasis, oxidative stress and neuroinflammation in the brain. Moreover, inflammatory, lipid metabolism and oxidative stress-related gut microbiota including Helicobacter, Colidextribacter, Anaerotruncus, Parasutterella, Allobaculum, Alloprevotella, Alistipes, Bifidobacterium and Candidatus_Saccharimonas were also regulated by TG-Res-CS/TPP-NPs. This work indicates the potential use of TG-Res-CS/TPP-NPs for the delivery of Res.

A Flower-like Brain Targeted Selenium Nanocluster Lowers the Chlorogenic Acid Dose for Ameliorating Cognitive Impairment in APP/PS1 Mice.

Aß aggregation-related neuroinflammation and imbalance of brain glucose homeostasis play important roles in the pathological process of Alzheimer's disease (AD). Chlorogenic acid (CGA) is one of the most common dietary polyphenols with neuroprotective effects. However, due to the low bioavailability of CGA, its application dose is usually high in vivo. In our previous study, the spherical selenium nanoparticles act as drug carriers to improve the bioactivity of resveratrol. Here, the brain-targeting peptide (TGN peptide) and CGA were used to prepare a new flowerlike selenium nanocluster (TGN-CGA@SeNCs) for enhancing the bioavailability of CGA. After decoration on selenium nanoclusters, the solubility and stability of CGA was obviously increased. Oral administration of a low dose of CGA (80 mg/kg/body weight) only slightly inhibited Aß aggregate-related neuroinflammation and glucose homeostasis disorder in the brain. Moreover, CGA showed less effect on increasing the diversity and richness of gut microbiota. At the same concentration, the CGA-modified selenium nanocluster (CGA@SeNCs) and TGN-CGA@SeNCs showed better function in ameliorating the gut microbiota disorder. Especially, TGN-CGA@SeNCs significantly increased the relative abundance of Turicibacter, Colidextribacter, Ruminococcus, Alloprevotella, and Alistipes against oxidative stress, inflammation, and glucose homeostasis imbalance. Notably, only TGN-CGA@SeNCs can transport through the blood-brain barrier (BBB), and TGN-CGA@SeNCs showed better effects than CGA@SeNCs in regulating Aß aggregation and improving brain glucose homeostasis. These results broadened the application of TGN-CGA@SeNCs, effectively improving the bioactivity of CGA, which also lowers the CGA dose for preventing AD progression.

Smilax china Polyphenols Stimulate Browning via [Formula: see text]3-Adrenergic Receptor/AMP-Activated Protein Kinase [Formula: see text] Signaling Pathway in 3T3-L1 Adipocytes.

The aim of this study is to investigate the molecular mechanism of Smilax china L. polyphenols (SCLPs) in enhancing lipid metabolism and stimulating browning to reduce lipid accumulation in 3T3-L1 adipocytes. SCLP treatment obviously decreased lipid content in a dose-dependent manner (10-40 µg/mL) in adipocytes. SCLP treatment cooperated with noradrenalin to increase lipolysis. SCLPs reduced the gene expressions of C/EBP[Formula: see text] and Ap2 and enhanced the expressions of ACO, CPT, pHSL/HSL, ATGL, and PKA in adipocytes. Furthermore, SCLPs increased mRNA and protein expressions of brown adipocyte-specific factors (UCP-1, PRDM16, PGC-1α, and PPARγ) and mRNA expressions of beige adipocyte-specific markers (CD137, Tbx1, and Tmem26) in 3T3-L1 adipocytes, as well as mitochondrial biogenesis genes (Nrf1 and Tfam). In addition, according to the immunofluorescence staining, the mitochondria number was increased by SCLP. Moreover, ß3-AR or AMPK agonist synergistic SCLPs enhanced the expressions of UCP-1, PRDM16, and PGC-1α. While ß3-AR or AMPK antagonist significantly decreased the expressions of these brown adipocyte-specific factors, SCLP treatment inhibited the effect of antagonist to improve the expression of UCP-1, PRDM16, and PGC-1α. These results indicated that SCLPs may regulate lipid metabolism and stimulate browning via the ß3-AR/AMPKα signaling pathway. Thus, SCLPs likely have potential therapeutic effects on obesity.

Multifunctional Selenium Nanoparticles with Different Surface Modifications Ameliorate Neuroinflammation through the Gut Microbiota-NLRP3 Inflammasome-Brain Axis in APP/PS1 Mice.

Neuroinflammation plays a critical role in Alzheimer's disease (AD). However, it is still unknown if neuroinflammation can be effectively treated using selenium nanoparticles (SeNPs) with different surface modifications. In this study, SeNPs were coated with dihydromyricetin (DMY), a natural polyphenol, to obtain DMY@SeNPs. Given that DMY@SeNPs are unstable under physiological conditions, they were decorated step-by-step with chitosan (CS/DMY@SeNPs) and with the blood brain barrier (BBB) targeting peptide Tg (TGNYKALHPHNG) to yield Tg-CS/DMY@SeNPs, which significantly reduced the aggregation of Aß and improved the anti-inflammatory effects of SeNPs in vitro. The mechanisms of CS/DMY@SeNPs and Tg-CS/DMY@SeNPs on regulating neuroinflammation are different. Only Tg-CS/DMY@SeNPs can cross the BBB; therefore, Tg-CS/DMY@SeNPs more successfully inhibited Aß aggregation and reduced inflammatory cytokine secretion via the NF-κB pathway in the brain of APP/PS1 mice compared to CS/DMY@SeNPs. Furthermore, both types of nanoparticles, however, were able to repair the gut barrier and regulate the population of inflammatory-related gut microbiota such as Bifidobacterium, Dubosiella, and Desulfovibrio. Of note, the relative abundance of Gordonibacter was only enhanced by Tg-CS/DMY@SeNPs, thereby downregulating the protein expression of the NLRP3 inflammasome and the concentrations of serum inflammatory factors. This demonstrates that Tg-CS/DMY@SeNPs ameliorate neuroinflammation through the gut microbiota-NLRP3 inflammasome-brain axis. Overall, our data suggest that Tg-CS/DMY@SeNPs are an ideal drug candidate for AD treatment.

Regulating the Imbalance of Gut Microbiota by Smilax china L. Polyphenols to Alleviate Dextran Sulfate Sodium-induced Inflammatory Bowel Diseases.

Smilax china L. is used not only as a kind of traditional Chinese herbal medicinal ingredients with various pharmacological properties, but also as food in certain parts of China. However, it is by far still unclear whether Smilax china L. polyphenols (SCP), as important bioactive constituents in Smilax china L., have effects on inflammatory bowel diseases (IBD). This study investigated the impact of SCP on the dextran sulfate sodium (DSS)-induced IBD and gut microbiota in mice. SCP treatments ameliorated typical symptoms of IBD as what was reflected through suppressing body weight loss, colonic shortening, intestinal barrier damage, and increasing intestinal disease activity index. SCP treatments simultaneously decreased the release of proinflammatory cytokines and oxidative stress, as well as promoted the release of anti-inflammatory factors. Furthermore, SCP ameliorated the ecological imbalance of gut microbiota and regulated the key bacteria associated with IBD (including Akkermansiaceae, Ruminococcaceae, Acidaminococcaceae, Muribaculaceae, and Anaeroplasmataceae). In general, SCP may improve DSS-induced IBD in mice by regulating inflammatory factors, inhibiting oxidative stress, reducing intestinal tissue damage, and regulating the ecological imbalance of intestinal microbiota. Thus, SCP might serve as a potential therapeutic agent against the inflammation-driven diseases.

Feasibility and efficacy of transthoracic single-port assisted laparoscopic esophagogastrectomy for Siewert type II adenocarcinoma of the esophagogastric junction.

BACKGROUND: The surgical treatment of Siewert type II adenocarcinoma of the esophagogastric junction (AEG) is controversial, and no systematic technology has been established. The aim of this retrospective study is to introduce the technology of transthoracic single-port assisted laparoscopic esophagogastrectomy. METHODS: Data from patients with Siewert type II AEG who underwent transthoracic single-port assisted laparoscopic esophagogastrectomy in Guangdong Provincial Hospital of Chinese Medicine from May 2017 to December 2020 were analyzed. RESULTS: A total of 35 patients, including 30 males and 5 females, were enrolled in this study. Eight patients underwent proximal gastrectomy while the other 27 patients underwent total gastrectomy. The median operative times were 247.5 (195.0-275.0) min and 290.0 (173.0-530.0) min for proximal and total gastrectomy, respectively. The median lower mediastinal lymph node dissection (LMLD) time was 41.5 (20.0-57.0) min and the median estimated blood loss was 100.0 (20.0-200.0) mL. The median number of harvested mediastinal lymph nodes was 5 [2-13]. Lower mediastinal lymph node metastasis occurred in 9 patients (25.7%). The lower mediastinal lymph node metastasis rate was significantly higher in patients with esophageal involvement exceeding 2 cm [>2 vs. ≤2 cm: 55.6% (5/9) vs. 15.4% (4/26), P=0.03]. The median postoperative hospital stay was 10 [6-73] days. Overall morbidity was 11.8% (4 patients), including 2 cases of pleural effusion, 1 case of pancreatic fistula, and 1 case of anastomotic leakage. CONCLUSIONS: Transthoracic single-port assisted laparoscopic esophagogastrectomy is safe and feasible. It has the advantages of reducing the difficulty of LMLD and digestive tract reconstruction.

Oral Administration of Resveratrol-Selenium-Peptide Nanocomposites Alleviates Alzheimer's Disease-like Pathogenesis by Inhibiting Aß Aggregation and Regulating Gut Microbiota.

Alzheimer's disease (AD) is a neurodegenerative disease associated with amyloid-ß (Aß) deposition, leading to neurotoxicity (oxidative stress and neuroinflammation) and gut microbiota imbalance. Resveratrol (Res) has neuroprotective properties, but its bioavailability in vivo is very low. Herein, we developed a small Res-selenium-peptide nanocomposite to enable the application of Res for eliminating Aß aggregate-induced neurotoxicity and mitigating gut microbiota disorder in aluminum chloride (AlCl3) and d-galactose(d-gal)-induced AD model mice. Res functional selenium nanoparticles (Res@SeNPs) (8 ± 0.34 nm) were prepared first, after which the surface of Res@SeNPs was decorated with a blood-brain barrier transport peptide (TGN peptide) to generate Res-selenium-peptide nanocomposites (TGN-Res@SeNPs) (14 ± 0.12 nm). Oral administration of TGN-Res@SeNPs improves cognitive disorder through (1) interacting with Aß and decreasing Aß aggregation, effectively inhibiting Aß deposition in the hippocampus; (2) decreasing Aß-induced reactive oxygen species (ROS) and increasing activity of antioxidation enzymes in PC12 cells and in vivo; (3) down-regulating Aß-induced neuroinflammation via the nuclear factor kappa B/mitogen-activated protein kinase/Akt signal pathway in BV-2 cells and in vivo; and (4) alleviating gut microbiota disorder, particularly with respect to oxidative stress and inflammatory-related bacteria such as Alistipes, Helicobacter, Rikenella, Desulfovibrio, and Faecalibaculum. Thus, we anticipate that Res-selenium-peptide nanocomposites will offer a new potential strategy for the treatment of AD.

A flavonoid-rich Smilax china L. extract prevents obesity by upregulating the adiponectin-receptor/AMPK signalling pathway and modulating the gut microbiota in mice.

The aim of this study was to investigate the effects of Smilax china L. flavonoid (SCF) on obesity and changes in gut microbiota high-fat/high-sucrose (HFHS)-fed mice. Male C57BL/6 mice fed either a normal-chow (NC) or a HFHS diet were treated with SCF for 12 weeks. The effect of SCF on the composition of gut microbiota was assessed by 16S rDNA sequencing. SCFA levels in the caecum were quantified by GC-MS. SCF supplementation alleviated the body weight gain, fat accumulation, serum lipid parameters, and hepatic steatosis and improved glucose homeostasis. SCF significantly increased plasma adiponectin level, adiponectin-receptor-gene (AdipoR1 and AdipoR2) expression in the liver, activated AMPKα, downregulated the expression of SREBP1-c, FAS, and ACCα, and upregulated the expression of PPARα, CPT-1α, and UCP-1. The anti-obesity effects of SCF might be through upregulation of adiponectin-receptor/AMPK signalling to improve lipid metabolism. SCF reversed HFHS-induced dysbiosis of gut microbiota and decreased SCFA production in the caecum, thus reducing energy absorption and leading to loss of body weight. Spearman's correlation analysis revealed significant correlations between obesity phenotypes, SCFA levels, and changes in gut microbiota. The results showed that SCF may be an effective dietary supplement that is useful for suppressing the development of obesity and associated disorders.

Chlorogenic acid and caffeine combination attenuates adipogenesis by regulating fat metabolism and inhibiting adipocyte differentiation in 3T3-L1 cells.

Obesity is a complex disease spreading in the world. In our previous studies, chlorogenic acid (CGA) and caffeine had ever been reported to reduce the body weight gain and fat accumulation in mice. This study investigated the anti-obesity effect of CGA and caffeine on 3T3-L1 cells. According to triglyceride (TG) assay and Oil-Red O staining, 40 µg/ml CGA and 160 µg/ml caffeine reduced TG content. Moreover, CGA + caffeine inhibited the mRNA expression of major adipogenic markers, PPAR-γ2, and C/EBPα in the metaphase and anaphase stages of differentiation induction (Day 2 and 4). CGA + caffeine improved P-AMPK/AMPK accompanied by decreasing the expression of GPDH and FAS to depress the lipid synthesis, increasing the mRNA expression of ACO and CAT to promote fatty acid oxidation and up-regulated the expression of hydrolysis-related enzyme adipose TG lipase (ATGL) and P-HSL/HSL. Furthermore, CGA + caffeine improved the expression of Glut4 which promoted the glucose transport. Taken together, these data demonstrated CGA + caffeine inhibited 3T3-L1 cells differentiation in the middle and late stages and reduced the fat accumulation through AMPK pathway by regulating the fat metabolism-related enzyme in 3T3-L1 cells to attenuates adipogenesis. PRACTICAL APPLICATIONS: The aim of this study was to elucidate the potential role of chlorogenic acid and caffeine in the treatment of obesity.

Astilbin lowers the effective caffeine dose for decreasing lipid accumulation via activating AMPK in high-fat diet-induced obese mice.

BACKGROUND: Caffeine has an anti-obesity effect, although chronic excessive caffeine consumption also causes caffeinism, which is marked by increased anxiety or depression, amongst other symptoms. The present study aimed to investigate whether the addition of flavonoids such as astilbin can reduce the caffeine dose needed to inhibit obesity. RESULTS: ICR mice (n = 80) were fed with normal diet, high-fat diet (HFD), HFD supplemented with astilbin, caffeine, or astilbin + caffeine for 12 weeks. When diets supplemented with astilbin, 0.3 g kg-1 diet caffeine had the same effect as 0.6 g kg-1 diet caffeine alone, and 0.6 g kg-1 diet caffeine combined with astilbin most effectively inhibited HFD-induced obesity. Astilbin improved the anti-obesity effects of caffeine on lipid accumulation via the activation of AMP-activated protein kinase α (AMPKα). (i) Activated AMPKα decreased lipid biosynthesis by suppressing the activity or mRNA expression of 3-hydroxy-3-methylglutaryl-CoA reductase, sterol regulatory element binding protein 1c and its target gene fatty acid synthase. (ii) Activated AMPKα also up-regulated lipolysis by enhancing the expression of adipose triglyceride lipase and increasing the phosphorylation of hormone-sensitive lipase. (iii) Finally, activated AMPKα increased carnitine acyltransferase and acyl-CoA oxidase activities, which further promoted fatty acid ß-oxidation. CONCLUSION: The results obtained in the present study indicate that astilbin may decrease the effective dose of caffeine needed for an anti-obesity effect and also suggest that it suppresses fat accumulation via the activation of AMPK. © 2020 Society of Chemical Industry.

Collaborative effects of chlorogenic acid and caffeine on lipid metabolism via the AMPKα-LXRα/SREBP-1c pathway in high-fat diet-induced obese mice.

To investigate the mechanism of the combined effects of chlorogenic acid (CGA) and caffeine on lipid metabolism in high-fat diet-induced obese mice, eighty female ICR mice were randomly divided into eight groups and fed with a high-fat diet with/without CGA and/or caffeine for 14 weeks. The combination of CGA and caffeine effectively decreased body weight gain, intraperitoneal adipose tissue weight, serum LDL-c, FFA, TC, TG, leptin, IL-6 concentrations, and hepatic TG and TC levels and increased the serum adiponectin level. The CGA and caffeine combination also promoted the phosphorylation of AMPKα, inhibited the expressions of transcriptional regulators (SREBP-1c and LXRα), and decreased the expressions of FAS and HMGR. Besides, the expressions of ACO, ATGL and HSL were increased by the CGA and caffeine combinations. The results indicated that the combination of CGA and caffeine had anti-obesity effects and regulated lipid metabolism in high-fat diet-induced obese mice via the AMPKα-LXRα/SREBP-1c signaling pathway. Thus, chronic CGA and caffeine intakes may be potent for preventing obesity.

Chemical composition, antibacterial properties, and mechanism of Smilax china L. polyphenols.

This work aimed at investigating the chemical composition, antibacterial properties, and effect mechanism of Smilax china L. polyphenols (SCLP). SCLP was extracted and purified, and then, its eighteen polyphenolic compounds were identified by LC-MS/MS analysis. SCLP exhibited antibacterial activity against five bacteria (Salmonella typhimurium, Listeria monocytogenes, Staphylococcus aureus, Bacillus subtilis, and Escherichia coli) with minimum inhibitory concentration in a range of 195.31 to 781.25 µg/mL. Escherichia coli and Staphylococcus aureus showed a higher sensitivity to SCLP. Notably, when combined with antibiotics, the SCLP-thiamphenicol and SCLP-gatifloxacin combinations showed additional properties against Escherichia coli and Staphylococcus aureus, while SCLP-streptomycin and SCLP-penicillin combinations exhibited dramatically synergistic effects. In addition, the changes in permeability and integrity of the cell membrane and cell wall were observed by measuring UV absorption, extracellular AKP concentration, FTIR spectroscopy, and scanning electron microscopy. It is speculated that the mechanism of action of SCLP on bacteria may be described as destruction of bacterial cell wall and cell membrane. In conclusion, SCLP was a potential natural antimicrobial substance with strong antimicrobial activity, which may reduce the use of antibiotics or combat drug-resistant bacteria through synergistic combination with antibiotics.

Effect of Smilax china L. starch on the gel properties and interactions of calcium sulfate-induced soy protein isolate gel.

Hydrocolloids have been widely used in the food industry as gelling agents, stabilizers and food thickeners to improve the viscosity, texture and stability of foods. Normally, individual polysaccharides or proteins do not form an excellent solid gel. Therefore, composite gels have received extensive attention. In this study, the effects of Smilax china L. starch (SCS) on the gel properties and interactions of CaSO4-induced soy protein isolate (SPI) gel was investigated. The gel properties of SCS-SPI gel system were analyzed by dynamic rheological, gel strength and water holding capacity. Synchronously, the interaction and microstructure of SCS-SPI gel system were evaluated by protein solubility and scanning electron microscope. Finally, the gel mechanism of the gel system was established. Viscosity, elasticity, gel strength and water holding capacity were obviously increased and microstructure become more compact of gel system and with the concentration increased of SCS. Furthermore, the result of protein solubility showed that hydrophobic, hydrogen bond and disulfide bond interaction play an important role on maintaining the gel system.

Dietary supplement of Smilax china L. ethanol extract alleviates the lipid accumulation by activating AMPK pathways in high-fat diet fed mice.

BACKGROUND: Obesity has become a public health concern worldwide because it is linked to numerous metabolic disorders, such as hyperlipidemia, hypertension and cardiovascular disease. Therefore, there is an urgent need to develop new therapeutic strategies that are efficacious and have minimal side effects in obesity treatment. This study examined the effect of dietary supplement of Smilax china L. ethanol extract (SCLE) on high-fat diet (HFD) induced obesity. METHODS: Fifty ICR mice were fed a normal diet, high-fat diet (HFD) or HFD supplemented with 0.25, 0.5% or 1% SCLE for 8 weeks. Body weight, intraperitioneal adipose tissue (IPAT) weight, serum biochemical parameters, and liver lipids were measured. Activity, mRNA and protein expressions of lipid metabolism-related enzymes were analyzed. RESULTS: Over 0.5% SCLE had reduced cholesterol biosynthesis by the activation of AMP-activated protein kinase (AMPK), which subsequently suppressed the mRNA expression of both sterol regulatory element binding protein-2 and 3-hydroxy-3-methyl-glutaryl-CoA reductase. Thus, the plasma and liver cholesterol concentrations in the HFD-fed mice were decreased. AMPK activation caused by SCLE also significantly upregulated lipolysis by enhancing adipose triglyceride lipase and hormone-sensitive lipase activities. This accelerated triglyceride hydrolysis and fatty acid release. Finally, SCLE increased carnitine palmitoyltransferase 1 and acyl-CoA oxidase activities, which further promoted fatty acid ß-oxidation. CONCLUSION: SCLE could lead to a decrease in body weight gain and fat mass by inhibiting the lipid synthesis and promoting lipolysis and ß-oxidation in HFD fed mice. The underlying mechanism is probably associated with regulating AMPK pathway.

Chemical composition, antioxidant activities of polysaccharide from Pine needle (Pinus massoniana) and hypolipidemic effect in high-fat diet-induced mice.

The aim of this study is to investigate hypolipidemic and antioxidant effects of Pine needle polysaccharide (PNP) from Pinus massoniana in high-fat diet (HFD)-induced mice. PNP could significantly improve the serum lipid levels (total cholesterol, triacylglycerols, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol), enhance the antioxidant enzymes levels (total antioxidant capability, superoxide dismutase, glutathione peroxidase, catalase), and decrease malondialdehyde (MDA) content in HFD-induced mice. PNP exhibited distinct antioxidant ability on the superoxide anions, 1, 1-diphenyl-2-picrylhydrazyl (DPPH) and ferric ion reducing antioxidant power (FRAP) in vitro. The average molecular weight (Mw) of PNP was 6.17 × 105 Da, and mainly of fucose, arabinose, galactose, glucose, galacturonic acid. These results suggested that PNP might be used as functional foods and natural drugs in enhancing antioxidant ability and alleviating the hyperlipidemia.

Enhanced Effect of Combining Chlorogenic Acid on Selenium Nanoparticles in Inhibiting Amyloid ß Aggregation and Reactive Oxygen Species Formation In Vitro.

The deposition of amyloid-ß (Aß) plaques and formation of neurotoxic reactive oxygen species (ROS) is a significant pathological signature of Alzheimer's disease (AD). Herein, a novel strategy is reported for combining the unique Aß absorption property of selenium nanoparticles with the natural antioxidant agent chlorogenic acid (CGA) to form CGA@SeNPs. The in vitro biological evaluation revealed that CGA could clear the ROS induced by Aß40 aggregates, but it did not inhibit the Aß40 aggregation and cell membrane damage which were also caused by Aß40 aggregates. Interestingly, CGA@SeNPs show an enhanced inhibition effect on Aß40 aggregation and, more importantly, protect PC12 cells from Aß aggregation-induced cell death. It is believed that CGA@SeNPs are more efficient than CGA in reducing Aß40 toxic in long-term use.

A comparative study of resveratrol and resveratrol-functional selenium nanoparticles: Inhibiting amyloid ß aggregation and reactive oxygen species formation properties.

Deposition of amyloid-ß (Aß) aggregates and formation of neurotoxic reactive oxygen species (ROS) are significant pathological signatures of Alzheimer's disease (AD). Resveratrol (Res) is an antioxidant with the potential to treat AD. However, the bioavailability and solubility of Res is very low and it cannot entirely inhibit Cu2+ -induced Aß42 aggregation at low concentration. Herein, we combine the unique Aß absorption property of selenium nanoparticles with the natural antioxidant agent Res to form Res@SeNPs. Our in vitro biological evaluation revealed that modification of Res with SeNPs provides a synergistic effect on Cu2+ -induced Aß42 aggregation, ROS generation and, more importantly, protects PC12 cells from Aß42-Cu2+ complexes-induced cell death. It is believed that SeNPs can improve the application of Res in AD treatment as Res@SeNPs is more efficient than Res in reducing Aß42 toxicity in long-term use. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 3034-3041, 2018.