To explore the protective effect of vitamin E (VE) against radiation injury of hippocampal neurons in mice and explore the possible mechanism.
 
  Cultured HT-22 and U251 cells with or without exposure to 8 Gy irradiation were treated with VE (200 μmol/L for 24 h), ferroptosis inhibitor (ferrostatin-1, 5 μmol/L for 24 h), apoptosis inhibitor (ZVAD-FMK, 2 μmol/L), or necroptosis inhibitor (100 μmol/L). MTT assay was used to evaluate the cell viability after the treatments, and reduced glutathione (GSH), malondialdehyde (MDA), lipid reactive oxygen species (lipid ROS), and intracellular iron ion levels were detected for assessment of ferroptosis. The mice exposed to 16 Gy irradiation with or without vitamin E (500 U/kg) treatment for 6 weeks were assessed for behavioral changes and cognitive functions using Morris water maze test.
 
  Treatment with VE significantly promoted the cell survival following irradiation in HT-22 cells (
  < 0.05) but not in U251 cells (
  > 0.05). Ferrostatin-1, but not ZVAD or the necroptosis inhibitor, promoted the survival of HT-22 cells following the irradiation. Exposure to irradiation significantly increased ferroptosis-related oxidative stress level in HT-22 cells, manifested by decreased GSH level and increased MDA, lipid ROS and intracellular iron ion levels (
  < 0.05); treatment with VE and ferrostatin-1 both obviously reversed radiation-induced ferroptosis-related oxidative stress in the cells (
  < 0.05). In Morris water maze test, the mice with radiation exposure showed obviously increased exploration time and distance (
  < 0.05), which were significantly decreased after treatment with VE (
  < 0.05).
 
  Vitamin E reduces radiation injury by inhibiting ferroptosis in the hippocampal neurons in mice.
 Vitamin E reduces radiation injury by inhibiting ferroptosis in the hippocampal neurons in mice.
  To investigate the inhibitory effect of ketogenic diet (KD) on growth of neuroblastoma in mice.
 
  BALB/c-nu mouse models bearing neuroblastoma xenografts were established by subcutaneous injection of human neuroblastoma cell line (SH-SY5Y). When the tumor volume reached 250 mm3, the mice were randomized into SD group with standard diet and PBS treatment, KD group with ketogenic diet and PBS treatment, and CP+KD group with ketogenic diet and cyclophosphamide (60 mg·kg
  ·day
  ) treatment, 
  =8. The tumor volume, body weight, blood glucose, ketone body (β-Hydroxybutyrate) levels, and hepatic steatosis in the mice were assessed. The expressions of caspase-3 and caspase-8 were detected by Western blotting, and Ki67 expresison was detected using immunohistochemistry (IHC). Transmission electron microscopy (TEM) was employed for the autophagosomes, and the autophagic protein Beclin1, LC3A/B and P62 were detected by IHC and Western blotting.
 
  On day 28 post tumor cell injection, the mice in KD and CP+KD groups couwith IHC.
 
  KD has a strong anti-tumor effect in the xenograft mouse model possibly by regulating cell autophagy.
 KD has a strong anti-tumor effect in the xenograft mouse model possibly by regulating cell autophagy.
  To explore the effect of 
  decoction (DGNTD) on cell apoptosis and TNF receptor super family 6 (Fas)/caspase-8 pathway in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS).
 
  FLS isolated from the synovial tissue of RA patients were cultured and identified using immunofluorescence staining. The cells were treated with 10% blank serum (blank control group), 10% sera containing low, moderate or high doses of DGNTD, or 20 μmol/mL KR-33493 (a Fas inhibitor) combined with 10% serum containing high-dose DGNTD. MTT assay was used to detect the proliferation of the cells after the treatments. Apoptosis of the cells was detected at 48 h in each group using Hoechst 33342 staining and flow cytometry with annexin V-FITC/PI staining. The mRNA and protein expressions of Fas, FADD, caspase-8 and caspase-3 in the cells at 48 h were detected using qPCR and Western blotting.
 
  Immunofluorescence staining identified the cultured cells as FLS. Treatment with DGNTD-containing sera significantly inhibited the proliferation of FLS, and the inhibitory effects were enhanced as the dose and intervention time increased (
  < 0.05).  https://www.selleckchem.com/products/nedometinib.html  Hoechst 33342 staining and flow cytometry showed that the sera containing different doses of DGNTD significantly promoted apoptosis of FLS (
  < 0.05). The expression levels of Fas, FADD, caspase-8, and caspase-3 at both mRNA and protein levels were significantly increased in the cells after treatment with different doses of DGNTD-containing sera (
  < 0.05). The application of KR-33493 obviously reversed the effects of DGNTD on the FLS (
  < 0.05).
 
  DGNTD can induce apoptosis of the FLS by activating Fas/caspase-8 signaling pathway.
 DGNTD can induce apoptosis of the FLS by activating Fas/caspase-8 signaling pathway.
  To explore the glucose-lowering effect of the polysaccharide fractions of 
  .
 
  The crude polysaccharides of 
  were chromatographed on DEAE cellulose column using H2O and 0.5 mol/L NaCl solution as the eluent and DEAE-water and DEAE-salt with high polysaccharide contents were collected. The two fractions were separated using Sephadex G-100 gel column to obtain 4 polysaccharide fractions TOPW-1, TOPW-2, TOPS-1, and TOPS-2. The anti-oxidation activity of the polysaccharide fractions was investigated with ABTS method. The fractions TOPW-1 and TOPS-1 with consistent UV detection signals were collected and HPGPC was used to determine their relative molecular mass. The monosaccharide composition in homogeneous TOPW-1 was determined by acid hydrolysis combined with HPLC. The 
  inhibitory activities of TOPW-1 and TOPS-1 against DPP4, adipocyte glucose intake and lipase activity were tested to preliminarily assess their glucose-lowering effect. In a mouse model of hyperglycemic and hyperlipidemic, the glucose-lowe, and their glucose-lowering effect is probably medicated by reducing oxidative stress and ameliorating lipid metabolism disorder.
 T. orientalis polysaccharides have anti-oxidation, glucose-lowering and lipid-lowering effects in mice, and their glucose-lowering effect is probably medicated by reducing oxidative stress and ameliorating lipid metabolism disorder.