Magnon Torque Transferred into a Magnetic Insulator through an Antiferromagnetic Insulator.

Electrical spin-orbit torque (SOT) in magnetic insulators (MI) has been intensively studied due to its advantages in spin-orbitronic devices with ultralow energy consumption. However, the magnon torque in the MIs, which has the potential to further lower the energy consumption, still remains elusive. In this work, we demonstrate the efficient magnon torque transferred into an MI through an antiferromagnetic insulator. By fabricating a Pt/NiO/Tm3Fe5O12 heterostructure with different NiO thicknesses, we have systematically investigated the evolution of the transferred magnon torque. We show that the magnon torque efficiency transferred through the NiO into the MI can retain a high value (∼50%), which is comparable to the previous report for the magnon torque transferred into the metallic magnet. Our study manifests the feasibility of realizing the pure magnon-based spin-orbitronic devices with ultralow energy consumption and high efficiency.

Apple polysaccharide protects ICR mice against colitis associated colorectal cancer through the regulation of microbial dysbiosis.

The study tried to investigate whether apple polysaccharide (AP) could prevent colitis associated colorectal cancer (CACC) through the regulation of intestinal microbiota disorders. 10 % AP (w/v) was administrated to ICR mice by gavage for 15 wk. It was found that AP treatment protected against CACC in mice effectively. The level of Lactobacillus in the intestine of AOM/DSS-treated mice was significantly decreased and that of Fusobacterium increased; while AP could reverse this trend and increase the intestinal microbiota diversity. The number of T cells and macrophages in the colon tissue of mice in AOM/DSS group elevated; while AP could reduce the number of these cells significantly. AP suppressed nuclear aggregation of ß-catenin, inhibited the activation of Wnt pathway in colon tissues. These data suggest that AP prevented ICR mice from CACC at least in part through regulating intestinal flora disorder and Wnt pathway.

Apple polysaccharide could promote the growth of Bifidobacterium longum.

It is widely accepted that regulating microbiome could improve human health. We previously observed apple polysaccharide (AP) reversed high-fat-induced microbial dysbiosis, but the mechanism remains to be elucidated. In this study, the function of AP in vitro was evaluated in Bifidobacterium longum (B. longum) and Lactobacillus rhamnosus (L. rhamnosus). The effects of AP on the composition of fecal bacteria of normal SD rats were investigated by qPCR, TA cloning and 16S sequencing. 0.125-2% AP showed no significant effect on the growth of B. longum and L. rhamnosus. DNA concentration of fecal bacteria cultured with 1% AP was significantly higher than that of control group. qPCR revealed that the number of Bifidobacterium and Lactobacillus in fecal flora incubated by 1% AP was significantly higher than that of control group. Three strains of escherichia coli (E. coli) in fecal bacteria were screened out and analyzed. AP can be utilized by one E. coli and the metabolic products of AP could enhance the proliferation of B. longum. These data suggest that AP could promote the growth of B. longum indirectly, and provide another basis to understand the health care function of apple.

Aralia taibaiensis Protects against I/R-Induced Brain Cell Injury through the Akt/SIRT1/FOXO3a Pathway.

BACKGROUND: Saponin from Aralia taibaiensis (sAT) showed excellent antioxidative effects in several models; however, its effects on brain cells were unknown to us. The present study was designed to evaluate the protective effects of sAT on ischemia/reperfusion- (I/R-) induced injury and clarify its mechanisms. METHODS: In vitro, HT22 cells were pretreated with sAT and then subjected to I/R. Apoptosis rate, mitochondrial function, and antioxidant proteins were measured. To clarify the mechanisms, siRNA were used. In vivo, sAT was pretreated through intragastric administration for 7 days and the I/R model was induced. The neurobehavioral scores, infarction volumes, and some cytokines in the brain were measured. Protein levels were investigated by Western blotting. RESULTS: The results showed that sAT treatment significantly protected cells from I/R-induced cell apoptosis and mitochondrial dysfunction. The antioxidant protein levels were increased in a dose-dependent manner. Further study revealed that sAT induced the deacetylation and phosphorylation of PGC-1α and FOXO3a. sAT treatment also induced the phosphorylation levels of Akt and the expression levels of SIRT1. Using the specific targeted siRNA transfection, the interplay relationship between Akt, SIRT1, PGC-1α, and FOXO3a was verified. Furthermore, the same protective effects were also observed in rats subjected to I/R. CONCLUSION: sAT protected brain cells from I/R-induced mitochondrial oxidative stress and dysfunction through regulating the Akt/SIRT1/FOXO3a/PGC-1α pathway.

UPLC-QTOF/MS-Based Metabolomics Reveals the Protective Mechanism of Hydrogen on Mice with Ischemic Stroke.

As a reductive gas, hydrogen plays an antioxidant role by selectively scavenging oxygen free radicals. It has been reported that hydrogen has protective effects against nerve damage caused by ischemia-reperfusion in stroke, but the specific mechanism is still unclear. Therefore, this study aims to investigate the protective effects of hydrogen on stroke-induced ischemia-reperfusion injury and its detailed mechanism. Two weeks after the inhalation of high concentrations (66.7%) of hydrogen, middle cerebral artery occlusion (MCAO) was induced in mice using the thread occlusion technique to establish an animal model of the focal cerebral ischemia-reperfusion. Then, a metabolomics analysis of mouse cerebral cortex tissues was first performed by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOF/MS) to study the metabolic changes and protective mechanisms of hydrogen on stroke ischemia-reperfusion injury. According to the metabolomic profiling of cortex tissues, 29 different endogenous metabolites were screened, including palmitoyl-L-carnitine, citric acid, glutathione, taurine, acetyl-L-carnitine, N-acetylaspartylglutamic acid (NAAG), L-aspartic acid, lysophosphatidylcholine (LysoPC) and lysophosphatidylethanolamine (LysoPE). Through pathway analysis, the metabolic pathways were concentrate on the glutathione pathway and the taurine pathway, mitochondrial energy metabolism and phospholipid metabolism that related to the oxidative stress process. This result reveals that hydrogen may protect against ischemic stroke by reducing oxidative stress during ischemia-reperfusion, thereby protecting nerve cells from reactive oxygen species(ROS).

Isoorientin alleviates UVB-induced skin injury by regulating mitochondrial ROS and cellular autophagy.

Ultraviolet B (UVB) irradiation increases the risk of various skin disorders, resulting in apoptosis, autophagy and oxidative stress and thereby promoting the risk of skin photoaging and carcinogenesis. The use of photochemoprotectors including natural products with antioxidant properties represents an effective strategy for preventing UVB-induced skin injury. Isoorientin (Iso), as a flavonoid compound, could be extracted from several plant species and possesses multiple biological activities. However, its role in regulating UVB-induced skin damage is little to be reported. In the study, we found that Iso treatment could protect human dermal fibroblasts (HDFs) against the effects of UVB irradiation by improving cell viability, suppressing MMP1 and MMP3 expression, inhibiting oxidative stress and inducing autophagy. In addition, Iso reduced UVB-triggered apoptosis, as evidenced by the decreased Caspase-3 activity in vitro. Furthermore, Iso was functioned as reactive oxygen species (ROS) scavenger that markedly hindered c-Jun N-terminal kinases (JNK) signaling activation in UVB-treated HFDs. Importantly, promoting JNK activity restored matrix metalloproteinase (MMP)-1/3 expression in Iso-incubated cells with UVB stimulation. Meanwhile, UVB exposure to the skin of mice and subsequent topical application of Iso delayed the progression of skin damage, resulting in autophagy and blocking the JNK activation and ROS production. In conclusion, these results indicated the photoprotective role of Iso and demonstrated that Iso could also be potentially used as an agent against UVB-stimulated skin damage.

Paris saponin VII extracted from trillium tschonoskii suppresses proliferation and induces apoptosis of human colorectal cancer cells.

ETHNOPHARMACOLOGICAL RELEVANCE: Saponins of many herbs could inhibit the growth of colorectal cancer cells. In the study, we investigated the effects of Paris saponin Ⅶ (PSⅦ), and elucidated its mechanism in colorectal carcinoma cells and a xenograft mouse model. MATERIALS AND METHODS: HT-29 and HCT-116 cells were treated with different concentrations of PSⅦ (0-100 µM). The effects of PSⅦ on HCT-116 cells were assessed using a microarray. Then, apoptotic cells were detected by flow cytometric analysis and apoptosis related protein expression was evaluated by Western blot. A xenograft model of nude mice was used to assess the effect of PSⅦ in vivo. RESULTS: MTT assay showed the IC50 values of PSⅦ for growth inhibition of HT-29 and HCT-116 cells were 1.02 ±â€¯0.05 µM and 3.50 ±â€¯0.79 µM respectively. Edu assay demonstrated that PSⅦ effectively suppressed the growth of HT-29 and HCT-116 cells. Treatment with 0-3 µM PSⅦ not only triggered apoptosis, but also activated caspase-3 and caspase-9 of HT-29 and HCT-116 cells in a concentration dependent manner. In parallel to the alterations, Bax and Cyto-c expression increased while Bcl-2 decreased. In nude mice, PSⅦ reduced the tumor size and induced the apoptosis of tumor cells. PSVII could suppress IL-6-induced phosphorylation of STAT3 in vitro and blocked STAT3 phosphorylation in vivo. CONCLUSION: Our results suggest that PSVII suppressed the activation of IL-6/STAT3 pathway, consequently suppressed the growth and proliferation and triggered the apoptosis of CRC cells. These findings indicate that PSⅦ might be an effective tumouristatic agent for the treatment of colorectal cancer.

Echinacoside alleviates hypobaric hypoxia-induced memory impairment in C57 mice.

Acute hypobaric hypoxia (HH) gives rise to persistent cognitive impairment, influencing memory function specifically. Echinacoside (ECH), one of the phenylethanoids isolated from the stems of Cistanche salsa, has been reported to prevent ischemia induced by neuronal injury traditionally. This study then tried to investigate whether ECH could alleviate HH-induced memory deficit. Ten C57 mice were used as control, and 50 were exposed to HH equivalent to 6,100 m for 7 days in a decompression chamber and were given ECH daily (50, 75, or 100 mg/kg) through gavage during the period of exposure. Cognitive performance was evaluated by the Morris water maze test. ECH, especially at 100 mg/kg, significantly reduced HH-induced memory decline. Furthermore, ECH increased the expression of nuclear factor E2 p45-related factor 2, heme oxygenase-1, NAD(P)H:quinone oxidoreductase 1, and γ-glutamyl cysteine synthetase in mRNA and protein levels, suggesting that the Keap1-Nrf2-ARE signaling pathway might be involved in neuronal adaptation. The results indicate that ECH could prevent HH-induced memory impairment, which is associated with antioxidant effect of ECH in the hippocampus.

Pantoprazole-induced acute kidney injury: A case report.

The present study reports a case of pantoprazole-induced acute kidney disease. The patient was diagnosed with acute kidney injury with wide interstitial inflammation and eosinophil infiltration. Following 1 month of glucocorticoid therapy, the patient's serum creatinine and urea nitrogen decreased to within normal ranges. The presentation, clinical course, diagnosis and prognosis of pantoprazole-induced acute kidney injury are discussed herein to highlight the importance of early and correct diagnosis for good prognosis. Disease characteristics include short-term increased serum creatinine levels that respond to glucocorticoid treatment. The patient had no history of chronic kidney disease or proteinuria and presented with increased serum creatinine following treatment with pantoprazole. Following the end of pantoprazole treatment, short-term RRT and long-term prednisolone was administered, then serum creatinine returned to normal. Pantoprazole-induced acute kidney injury is commonly misdiagnosed and late diagnosis results in poor patient prognoses. Misdiagnosis leads to the administration of treatments that may exacerbate the condition, so appropriate diagnosis and treatment for pantoprazole-induced acute kidney injury is necessary.