Improvement of pasting and gelling properties of potato starch using a direct vapor-heat moisture treatment.

Conventional hydrothermal methods are lengthy and require high energy consumption. In this study, a quick and energy-saving direct vapor-heat moisture treatment (DV-HMT) method was used to improve the pasting and gelling properties of potato starch under the condition of high temperature (130 °C) and short periods (1, 3, 5, and 7 min). X-ray diffraction analysis exhibited that the relative crystallinity of DV-HMT starches decreased with the extension of treatment time. Small angle X-ray scattering measurements showed that the average thickness of the crystalline lamellae decreased from 6.193 to 5.937 nm, while the average thickness of the amorphous lamellae increased from 3.160 to 3.395 nm. Rapid visco-analyzer measurements exhibited that the breakdown values decreased to 0 mPa s for DV-HMT starches, indicating that this hydrothermal treatment led to starches with high resistance to heating and shearing. The gel hardness of starch treated by DV-HMT for 3 min (266 g) was around 5.4-fold higher than for non-treated starch (41 g). Considering the simple operation of DV-HMT and the short treatment periods (≤ 7 min) used in this study, DV-HMT could be a superior option to enhance the physicochemical and functional properties of starch.

Comparison of Lutein Bioaccessibility from Dietary Supplement-Excipient Nanoemulsions and Nanoemulsion-Based Delivery Systems.

The impact of lutein-loaded nanoemulsions and excipient nanoemulsions mixed with lutein-based dietary supplements (capsules and soft gels) on the bioaccessibility of lutein was explored using a simulated gastrointestinal tract (GIT). The particle size, particle size distribution, ζ-potential, microstructure, lipid digestibility, and lutein bioaccessibility of all the samples were measured after they were exposed to different environments (stomach and small intestine environments) within a simulated GIT. As expected, the bioaccessibility of lutein from the capsules (1.5%) and soft gels (3.2%) was relatively low when they were administered alone. However, the co-administration of excipient nanoemulsions significantly increased the bioaccessibility of lutein from both the capsules (35.2%) and soft gels (28.7%). This phenomenon was attributed to the fast digestion of the small oil droplets in the excipient nanoemulsions and the further formation of mixed micelles to solubilize any lutein molecules released from the supplements. The lutein-loaded nanoemulsions exhibited a much higher lutein bioaccessibility (86.8%) than any of the supplements, which was attributed to the rapid release and solubilization of lutein when the lipid droplets were rapidly and extensively digested within the small intestine. This study indicates that the bioaccessibility of lutein is much higher in nanoemulsion droplets than that in dietary supplements. However, consuming dietary supplements in the presence of nanoemulsion droplets can greatly increase lutein bioavailability. The results of this study have important guiding significance for the design of more effective lutein supplements.

Flavonoids of Rosa roxburghii Tratt exhibit radioprotection and anti-apoptosis properties via the Bcl-2(Ca(2+))/Caspase-3/PARP-1 pathway.

The objective of our study was to assess the radioprotective effect of flavonoids extracted from Rosa roxburghii Tratt (FRT) and investigate the role of Bcl-2(Ca(2+))/Caspase-3/PARP-1 pathway in radiation-induced apoptosis. Cells and mice were exposed to (60)Co γ-rays at a dose of 6 Gy. The radiation treatment induced significant effects on tissue pathological changes, apoptosis, Ca(2+), ROS, DNA damage, and expression levels of Bcl-2, Caspase-3 (C-Caspase-3), and PARP-1. The results showed that FRT acted as an antioxidant, reduced DNA damage, corrected the pathological changes of the tissue induced by radiation, promoted the formation of spleen nodules, resisted sperm aberration, and protected the thymus. FRT significantly reduced cell apoptosis compared with the irradiation group. The expression of Ca(2+) and C-Caspase-3 was decreased after FRT treatment compared with the radiation-treated group. At the same time, expression of prototype PARP-1 and Bcl-2 increased, leading to a decrease in the percentage of apoptosis cells in FRT treatment groups. We conclude that FRT acts as a radioprotector. Apoptosis signals were activated via the Bcl-2(Ca(2+))/Caspase-3/PARP-1 pathway in irradiated cells and FRT inhibited this pathway of apoptosis by down-regulation of C-Caspase-3 and Ca(2+) and up-regulation of prototype PARP-1 and Bcl-2.

Neuroprotective Effects of Icariin on Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice.

AIMS: This study investigated the neuroprotective properties of icariin (an effective component of traditional Chinese herbal medicine Epimedium) on neuronal function and brain energy metabolism maintenance in a triple-transgenic mouse model of Alzheimer's disease (3 × Tg-AD). METHODS: 3 × Tg-AD mice as well as primary neurons were subjected to icariin treatment. Morris water maze assay, magnetic resonance spectroscopy (MRS), Western blotting, ELISA, and immunohistochemistry analysis were used to evaluate the effects of icariin administration. RESULTS: Icariin significantly improved spatial learning and memory retention in 3 × Tg-AD mice, promoted neuronal cell activity as identified by the enhancement of brain metabolite N-acetylaspartate level and ATP production in AD mice, preserved the expressions of mitochondrial key enzymes COX IV, PDHE1α, and synaptic protein PSD95, reduced Aß plaque deposition in the cortex and hippocampus of AD mice, and inhibited ß-site APP cleavage enzyme 1 (BACE1) expression. Icariin treatment also decreased the levels of extracellular and intracellular Aß1-42 in 3 × Tg-AD primary neurons, modulated the distribution of Aß along the neurites, and protected against mitochondrial fragmentation in 3 × Tg-AD neurons. CONCLUSIONS: Icariin shows neuroprotective effects in 3 × Tg-AD mice and may be a promising multitarget drug in the prevention/protection against AD.

NADP(+)-IDH Mutations Promote Hypersuccinylation that Impairs Mitochondria Respiration and Induces Apoptosis Resistance.

Elucidating the tumorigenic mechanism of R-2-hydroxyglutarate (R-2HG) is critical for determining how NADP(+)-IDH mutations cause cancer. Here we report that R-2HG induces cancerous metabolism and apoptosis resistance through promoting hypersuccinylation. By competitive inhibition of the mitochondrial tricarboxylic acid cycle enzyme succinate dehydrogenase (SDH), R-2HG preferentially induced succinyl-CoA accumulation and hypersuccinylation in the mitochondria. IDH1 mutation-bearing glioma samples and cells were hypersuccinylated in the mitochondria. IDH1 mutation or SDH inactivation resulted in hypersuccinylation, causing respiration inhibition and inducing cancerous metabolism and mitochondrial depolarization. These mitochondrial dysfunctions induced BCL-2 accumulation at the mitochondrial membrane, leading to apoptosis resistance of hypersuccinylated cells. Relief of hypersuccinylation by overexpressing the desuccinylase SIRT5 or supplementing glycine rescued mitochondrial dysfunctions, reversed BCL-2 accumulation, and slowed the oncogenic growth of hypersuccinylated IDH1(R132C)-harboring HT1080 cells. Thus, R-2HG-induced hypersuccinylation contributes to the tumorigenicity of NADP(+)-IDH mutations, suggesting the potential of hypersuccinylation inhibition as an intervention for hypersuccinylation-related tumors.

Flavonoids of Rosa roxburghii Tratt act as radioprotectors.

BACKGROUND: To study the radioprotective effects of flavonoids from Rosa roxburghii Tratt (FRT). MATERIALS AND METHODS: The radioprotective effects of FRT were investigated by examining cell viability, 30-day survival of mice and the number of colony-forming units in spleen (CFU-S) after total-body 60Co irradiation. RESULTS: The survival rates of irradiated cells gradually increased with increasing concentrations of FRT. The survival rate was the highest at 87% with a concentration of 30 µg/mL. Pretreatment with FRT was needed to realize its radioprotective activity in mice at the dose of 60 mg/kg. With the increasing doses of 30 mg/kg, 60 mg/kg and 120 mg/kg, the numbers of CFU-S increased, and were significantly different compared with the control group. CONCLUSIONS: Pretreatment with FRT prior to irradiation resulted in significantly higher cell survival at 24 h after 5 Gy radiation, increased 30-day survival in mice after exposure to a potentially lethal dose of 8 Gy, and resulted in a higher number of CFU-S in mice after exposure to a dose of 6 Gy. These results collectively indicate that FRT is an effective radioprotective agent.

A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis.

The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1ß levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug.

Epidemiology of drug-induced liver injury in China: a systematic analysis of the Chinese literature including 21,789 patients.

BACKGROUND: The epidemiology of drug-induced liver injury (DILI) in China has rarely been studied before. The aim of the present study was to determine the etiology of DILI in a Chinese population by reporting a systematic analysis of the Chinese literature published from 1994 to 2011. METHODS: A comprehensive database search of the Chinese literature was performed to obtain all the relevant studies. The data, including the drug names and patients' sex, age, clinical classification, and prognosis, were collected and analyzed. RESULTS: In this research, we found 279 studies including 24 112 patients. There were 265 studies that reported the sex of 21 789 patients, 11 787 men and 10 002 women. The therapeutics included (but were not limited to) tuberculostatics, complementary and alternative medicines (CAMs), antibiotics, NSAIDs, antineoplastics, central nervous system agents, antithyroid drugs, and immunomodulators. Of these drugs, tuberculostatics and CAMs were the most common etiologies of DILI in China. CONCLUSION: DILI in China has a different etiology from that in Europe and USA. NSAIDs, which are the most common causes of DILI in western populations, are uncommon in China. Therefore, government, physicians, and patients should pay more attention to these drugs in DILI.