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Diffusion Tensor Imaging with the Dentate Nucleus After Repeated Management associated with Gadobutrol in youngsters.
However, FA ameliorated these hazardous effects in the antioxidant and anti-inflammatory systems in MTX-treated groups. Conclusion Based on our findings, oxidative stress impairment and MTX-induced liver damage were ameliorated following FA pretreatment at both histological and biochemical levels. Therefore, FA can be effectively used in abrogation of MTX-induced toxicity.Purpose Arsenic trioxide (ATO) has been shown to induce hepatic injury. Crocetin is a primary constituent of saffron, which has been verified to have antioxidant and anti-inflammatory effects. In the current experiment, we evaluated the efficacy of crocetin against ATO-induced hepatic injury and explored the potential molecular mechanisms in rats. Methods Rats were pretreated with 25 or 50 mg/kg crocetin 6 h prior to treating with 5 mg/kg ATO to induce hepatic injury daily for 7 days. Results Treatment with crocetin attenuated ATO-induced body weight loss, decreases in food and water consumption, and improved ATO-induced hepatic pathological damage. Crocetin significantly inhibited ATO-induced alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) increases. Crocetin prevented ATO-induced liver malondialdehyde (MDA) and reactive oxygen species (ROS) levels. Crocetin abrogated the ATO-induced decrease of catalase (CAT) and superoxide dismutase (SOD) activity. Crocetin was found to significantly restore the protein levels of interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor-alpha (TNF-α). Furthermore, crocetin promoted the expression of nuclear factor erythroid 2 related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NADP(H) quinone oxidoreductase 1 (NQO1). Conclusion These findings suggest that crocetin ameliorates ATO-induced hepatic injury in rats. In addition, the effect of crocetin might be related to its role in antioxidant stress, as an anti-inflammatory agent, and in regulating the Nrf2 signaling pathway.Purpose The aim of the present study was to investigate the interactions of the main components of Lygodium root (ie, p-coumaric acid, acacetin, apigenin, buddleoside and Diosmetin-7-O-β-D-glucopyranoside) with cytochrome P450 3A enzyme activity both in vitro and in vivo. Methods In vitro inhibition of drugs was assessed by incubating rat liver microsomes (RLMs) with a typical P450 3A enzyme substrate, midazolam, to determine their 50% inhibitory concentration (IC50) values. For the in vivo study, healthy male Sprague Dawley rats were consecutively administered acacetin or apigenin for 7 days at the dosage of 5 mg/kg after being randomly divided into 3 groups Group A (control group), Group B (acacetin group) and Group C (apigenin group). Results Among the five main components of Lygodium root, only acacetin and apigenin showed inhibitory effects on the cytochrome P450 3A enzyme in vitro. The IC50 values of acacetin and apigenin were 58.46 μM and 8.20 μM, respectively. Additionally, the in vivo analysis results revealed that acacetin and apigenin could systemically inhibit midazolam metabolism in rats. AZD4573 nmr The Tmax, AUC(0-t) and Cmax of midazolam in group B and group C were significantly increased (P less then 0.05), accompanied by a significant decrease in Vz/F and CLz/F (P less then 0.05). Conclusion Acacetin and apigenin could inhibit the activity of the cytochrome P450 3A enzyme in vitro and in vivo, indicating that herbal drug interactions might occur when taking Lygodium root and midazolam synchronously.Introduction Bladder cancer is a lethal human malignancy. Currently, treatment for bladder cancer is limited. The anti-tumor effects of leflunomide have attracted much more concern in multiple human cancers. Materials and methods This study evaluated the anti-tumor effects of leflunomide on cell viability, colony formation, apoptosis, and cell cycle in two human bladder carcinoma cell lines, 5637 and T24. Meanwhile, the underlying mechanism including PI3K/Akt signaling pathway and autophagy modulation was also identified. Results Leflunomide markedly inhibited the growth of both bladder cancer cell lines and induced apoptosis and cell cycle arrest in S phase. The phosphorylation levels of Akt and P70S6K in both cell lines were significantly down-regulated with leflunomide treatment. Furthermore, the deceased formation of autophagosomes and the accumulation of LC3II and P62 suggested the blockade of autophagy by leflunomide. Modulation of autophagy with rapamycin and chloroquine markedly attenuated and enhanced the cytostatic effects of leflunomide, respectively. Conclusion Leflunomide significantly reduced the cell viability of bladder cancer cells via inducing apoptosis and cell cycle arrest and suppressing the PI3K/Akt signaling pathway. In addition, the blockade of autophagy was observed, and autophagy inhibition enhanced leflunomide-mediating anti-tumor effects. Our data presented here offer novel ideas for comprehensive therapeutic regimes on bladder cancer.Purpose Diagnostic 24-hour intraocular pressure curves (IPC) are well established in the management of glaucoma. However, objective criteria for the IPC indication are lacking. The aim of this study was to evaluate the impact of individual patient characteristics and glaucoma-related parameters on therapy decisions after IPC and thus examine their relevance for glaucoma management. Patients and methods Retrospective analysis of adult primary open-angle glaucoma (POAG) patients who underwent an IPC (≥6 IOP measurements in 24 hours). The main exclusion criterion was previous IOP-lowering surgery. IPC-dependent (eg, mean and peak IOP) and IPC-independent parameters (eg, perimetry, RNFL thickness) were analyzed in relation to the therapeutic decision after IPC. Further, these parameters were compared in patient subgroups based on age, glaucoma stage, or therapy intensity. Results A total of 101 eyes of 101 patients were included. In general, mean and peak IOP were elevated in patients with a therapeutic change after IPC. These subjects presented differences of IPC-independent parameters (eg, IOP at admission, RNFL thickness, glaucoma stage). Regression analysis results suggested a predictive role of IPC-independent parameters for IPC therapeutic decisions. In subgroups of patients of older age or advanced glaucoma, IPC-independent parameters did not correlate with therapeutic decisions after IPC. Conclusion These results support the relevance of IPC in the therapeutic management of POAG. Moreover, the study promotes a personalized classification of patients using selected glaucoma characteristics to objectivize their individual benefit from IPC. Further prospective studies are needed to verify the utility of these parameters and IPC in the management of glaucoma.
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