Chemical Constituents, Hypolipidemic, and Hypoglycemic Activities of Edgeworthia gardneri Flowers.

The flowers of Edgeworthia gardneri are used as herbal tea and medicine to treat various metabolic diseases including hyperglycemia, hypertension, and hyperlipidemia. This paper investigate the chemical constituents and biological activities of ethanolic extract and its different fractions from E. gardneri flowers. Firstly, the E. gardneri flowers was extracted by ethanol-aqueous solution to obtain crude extract (CE), which was subsequently fractionated by different polar organic solution to yield precipitated crystal (PC), dichloromethane (DCF), ethyl acetate (EAF), n-butanol (n-BuF), and residue water (RWF) fractions. UHPLC-ESI-HRMS/MS analysis resulted in the identification of 25 compounds, and the main compounds were flavonoids and coumarins. The precipitated crystal fraction showed the highest phenolic and flavonoid contents with 344.4 ± 3.38 mg GAE/g extract and 305.86 ± 0.87 mg RE/g extract. The EAF had the strongest antioxidant capacity and inhibitory effect on α-glucosidase and pancreatic lipase with IC50 values of 126.459 ± 7.82 and 23.16 ± 0.79 µg/mL. Besides, both PC and EAF significantly regulated the glucose and lipid metabolism disorders by increasing glucose consumption and reducing TG levels in HepG2 cells. Molecular docking results suggested that kaempferol-3-O-glucoside and tiliroside had good binding ability with enzymes, indicating that they may be potential α-glucosidase and pancreatic lipase inhibitors. Therefore, the E. gardneri flowers could be served as a bioactive agent for the regulation of metabolic disorders.

Confusoside from Anneslea fragrans Alleviates Acetaminophen-Induced Liver Injury in HepG2 via PI3K-CASP3 Signaling Pathway.

Confusoside (CF), a major chemical compound in the leaves of Anneslea fragrans Wall., is a dihydrochalcone glycoside with excellent antioxidant and anti-inflammatory effects. However, the hepatoprotective effect of CF has not been described. This study aimed to explore the hepatoprotective effect of CF against acetaminophen (APAP)-induced hepatic injury in HepG2 cells. First, the potential hepatoprotective effect mechanisms of CF were predicted by network pharmacology and were thought to involve reducing inflammation and inhibiting apoptosis. Target proteins (phosphatidylinositol3-kinase (PI3K) and caspase-3 (CASP3)) were found via molecular docking analysis. To verify the predicted results, an analysis of biological indicators was performed using commercial kits and Western blotting. The results showed that CF significantly decreased the levels of liver injury biomarkers (ALT, AST, and LDH), strongly inhibited the production of inflammatory cytokines (IL-1ß, IL-6, and TNF-α) and the NO level via inhibiting the activation of the NF-κB signaling pathway, and markedly regulated the expression levels of Bcl2, Bax, and cleaved-CASP3/9 proteins by activating the PI3K-CASP3 apoptosis pathway. The results demonstrated that CF has a therapeutic effect on APAP-induced liver injury by inhibiting intracellular inflammation and cell apoptosis, indicating that CF may be used as a potential reagent for the prevention and treatment of APAP-induced liver injury.

Stability simulation analysis of targeted puncture in L4/5 intervertebral space for PELD surgery.

Introduction: The application prospects of percutaneous endoscopic lumbar discectomy (PELD) as a minimally invasive spinal surgery method in the treatment of lumbar disc herniation are extensive. This study aims to find the optimal entry angle for the trephine at the L4/5 intervertebral space, which causes less lumbar damage and has greater postoperative stability. To achieve this, we conduct a three-dimensional simulated analysis of the degree of damage caused by targeted puncture-based trephine osteotomy on the lumbar spine. Methods: We gathered clinical CT data from patients to construct a lumbar model. This model was used to simulate and analyze the variations in trephine osteotomy volume resulting from targeted punctures at the L4/5 interspace. Furthermore, according to these variations in osteotomy volume, we created Finite Element Analysis (FEA) models specifically for the trephine osteotomy procedure. We then applied mechanical loads to conduct range of motion and von Mises stress analyses on the lumbar motion unit. Results: In percutaneous endoscopic interlaminar discectomy, the smallest osteotomy volume occurred with a 20° entry angle, close to the base of the spinous process. The volume increased at 30° and reached its largest at 40°. In percutaneous transforaminal endoscopic discectomy, the largest osteotomy volume was observed with a 50° entry angle, passing through the facet joints, with smaller volumes at 60° and the smallest at 70°. In FEA, M6 exhibited the most notable biomechanical decline, particularly during posterior extension and right rotation. M2 and M3 showed significant differences primarily in rotation, whereas the differences between M3 and M4 were most evident in posterior extension and right rotation. M5 displayed their highest stress levels primarily in posterior extension, with significant variations observed in right rotation alongside M4. Conclusion: The appropriate selection of entry sites can reduce lumbar damage and increase stability. We suggest employing targeted punctures at a 30° angle for PEID and at a 60° angle for PTED at the L4/5 intervertebral space. Additionally, reducing the degree of facet joint damage is crucial to enhance postoperative stability in lumbar vertebral motion units.

Breast cancer and background parenchymal enhancement at breast magnetic resonance imaging: a meta-analysis.

BACKGROUND: The background parenchymal enhancement at breast magnetic resonance imaging use to predict breast cancer attracts many searchers to draw a possible relationship. However, the results of their relationships were conflicting. This meta-analysis was performed to assess breast cancer frequency associations with background parenchymal enhancement. METHODS: A systematic literature search up to January 2020 was performed to detect studies recording associations between breast cancer frequency and background parenchymal enhancement. We found thirteen studies including 13,788 women at the start with 4046 breast cancer. We calculated the odds ratio (OR) and the 95% confidence intervals (CIs) between breast cancer frequency and background parenchymal enhancement by the dichotomous technique with a random or fixed-effect model. RESULTS: Women with minimal or mild background parenchymal enhancement at breast magnetic resonance imaging did not have any risk of breast cancer compared to control women (OR, 1.20; 95% CI 0.54-2.67). However, high background parenchymal enhancement at breast magnetic resonance imaging (OR, 2.66; 95% CI 1.36-5.19) and moderate (OR, 2.51; 95% CI 1.49-4.21) was associated with a significantly higher rate of breast cancer frequency compared to control women. CONCLUSIONS: Our meta-analysis showed that the women with high and moderate background parenchymal enhancement at breast magnetic resonance imaging have higher risks, up to 2.66 fold, of breast cancer. We suggest that women with high or moderate background parenchymal enhancement at breast magnetic resonance imaging to be scheduled for more frequent follow-up and screening for breast cancer to avoid any complications.

RPW8.1 enhances the ethylene-signaling pathway to feedback-attenuate its mediated cell death and disease resistance in Arabidopsis.

The Arabidopsis RESISTANCE TO POWDERY MILDEW 8.1 (RPW8.1) activates confined cell death and defense against different pathogens. However, the underlying regulatory mechanisms still remain elusive. Here, we show that RPW8.1 activates ethylene signaling that, in turn, negatively regulates RPW8.1 expression. RPW8.1 binds and stabilizes 1-aminocyclopropane-1-carboxylate oxidase 4 (ACO4), which may in part explain increased ethylene production and signaling in RPW8.1-expressing plants. In return, ACO4 and other key components of ethylene signaling negatively regulate RPW8.1-mediated cell death and disease resistance via suppressing RPW8.1 expression. Loss of function in ACO4, EIN2, EIN3 EIL1, ERF6, ERF016 or ORA59 increases RPW8.1-mediated cell death and defense response. By contrast, overexpression of EIN3 abolishes or significantly compromises RPW8.1-mediated cell death and disease resistance. Furthermore, ERF6, ERF016 and ORA59 appear to act as trans-repressors of RPW8.1, with OAR59 being able to directly bind to the RPW8.1 promoter. Taken together, our results have revealed a feedback regulatory circuit connecting RPW8.1 and the ethylene-signaling pathway, in which RPW8.1 enhances ethylene signaling, and the latter, in return, negatively regulates RPW8.1-mediated cell death and defense response via suppressing RPW8.1 expression to attenuate its defense activity.