Background: In this study, the clinical effect of lamivudine combined with leflunomide and methylprednisolone in the treatment of hepatitis B virus-associated glomerulonephritis (HBV-GN) and their influence on renal function indexes was explored. Methods: Patients with HBV-GN were selected for retrospective analysis and divided into the group B and group A, with 41 cases in each group. The group B was given leflunomide and methylprednisolone, whereas the group A was supplemented with lamivudine. The level of 24 h proteinuria (PRO), albumin (ALB), beta2-microglobulin (β2-MG), alanine aminotransferase (ALT), interferon-gamma (IFN-γ) and interleukin-4 (IL-4) in two groups was measured. The clinical efficacy, adverse reactions appetite, spirit, sleep and daily life scores of the two groups were recorded. Results: With the extension of treatment time to end of the treatment, the level of 24 h PRO, ALB and β2-MG in the group A significantly changed compared with that before treatment (p < 0.05). Moreover, the level of ALT, IFN-γ and IL-4 in the two groups significantly decreased compared with that before treatment, and the level of the three indexes in the group A decreased more significantly (p < 0.05). The total effective rate in the group A was higher than that in the group B (p < 0.05). The occurrence of adverse reactions showed no statistically significant difference between the two groups. After treatment, scores of appetite, spirit, sleep and daily living were increased in the two groups, and the increase in the group A was more significant than that in the group B (p < 0.05). Conclusions: Lamivudine combined with methylprednisolone and leflunomide treatment is conducive to clearing Hepatitis B virus (HBV) and improving renal function.
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
The authors investigated the effect of herbal medicine Schisandra chinensis extract (SchE) and Ginkgo biloba extract (GBE) on the oral pharmacokinetics of P-glycoprotein substrate talinolol in humans.Twelve healthy male volunteers took a single 100-mg oral dose of talinolol either alone or after pretreatment with 300 mg SchE twice daily or with 120 mg GBE three times daily for 14 days. On day 14, a single 100-mg oral dose of talinolol was administered. Plasma concentrations of talinolol from zero to 24 h were measured by high-performance liquid chromatography. SchE increased the area under the curve (AUC)0–24 of talinolol by 47% (90% confidence interval (CI), 18–84%; p = 0.010), and GBE by 21% (90% CI = 11–32%; p = 0.002). The Cmax of talinolol increased by 51% (90% CI = 21–89%; p = 0.007) with SchE treatment and by 33% (90% CI = 18–51%; p = 0.002) with GBE treatment, respectively. The t1/2 of talinolol increased by 7% (90% CI = −4% to 19%; p = 0.320) with SchE treatment and by 11% (90% CI = −12% to 38%; p = 0.436) with GBE treatment, respectively.The results suggest that both SchE and GBE significantly inhibited P-glycoprotein in humans. Patients receiving either SchE or GBE may require dose adjustments when treated with drugs primarily transported by P-glycoprotein.
Purpose: To determine the potential effect of ruscogenin in cisplatin-induced nephrotoxicity.
Methods: Rat renal tubular epithelial cells (NRK-52E) were treated with 50 μM cisplatin to establish an in vitro cell model of nephrotoxicity. Cytotoxicity was assessed by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, flow cytometry, and western blot. Different concentrations of ruscogenin (2.5, 5, and 10 μM) were incubated with cisplatin-treated NRK-52E cells. Alterations in the nod-like receptor family, the pyrin domain-containing protein (NLRP3) inflammasome, toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB), and nuclear factor erythropoietin-2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) components were determined using western blot. Flow cytometry was also used to investigate the levels of reactive oxygen species (ROS).
Results: Ruscogenin significantly increased cell viability (p < 0.01) and suppressed apoptosis of NRK- 52E cells (p < 0.01), attenuating cisplatin-induced cytotoxicity. The NLRP3 inflammasome was activated in cisplatin-treated NRK-52E cells with enhanced NLRP3, interleukin 1 beta, and cleaved caspase-1; however, ruscogenin significantly decreased the expression of NLRP3 inflammasome components (p < 0.01). Ruscogenin attenuated cisplatin-induced expression of TLR4, myeloid differentiation primary response 88, and NF-κB. Further, cisplatin induction enhanced ROS formation, with increased malondialdehyde and decreased glutathione reductase and catalase levels. Ruscogenin attenuated cisplatin-induced ROS accumulation in NRK-52E cells through up-regulation of Nrf2 and HO-1.
Conclusion: Ruscogenin protects against cisplatin-induced apoptosis, inflammation, and oxidative stress in renal tubular epithelial cells via suppression of TLR4/NF-κB activation and promotion of Nrf2/HO-1 activation. Therefore, ruscogenin provides a potential therapeutic strategy for mitigating cisplatin-induced nephrotoxicity.
Neuroplastin 65 (Np65) is a brain‐specific cell adhesion molecule that is highly expressed in the hippocampus, amygdala, and cortex, regions of the brain that are associated with memory and emotions. However, the role of Np65 in regulation of emotional behavior is still unclear. In the present study, we show that Np65 knock‐out (Np65 KO ) mice display enhanced anxiety‐like behavior, a reduction in some aspects of depressive‐like behaviors, and increased sociability and memory. Biochemical investigations revealed that Np65 KO mice show increased adult‐born neurons and proliferation in the hippocampus. In addition, the level of 5‐hydroxytryptamine (5‐ HT ) in the hippocampus was reduced. The expression of tryptophan hydroxylase 2 in the brainstem and the expression of the 5‐ HT 3A receptor were also decreased. Electrophysiological recordings confirmed an impaired maintenance of long‐term potentiation in the hippocampus of Np65 KO mice. Together, our findings uncover a role for Np65 in regulating anxiety‐ and depressive‐like behaviors and suggest that Np65 may be essential for the maintenance of emotional stability, indicating that it might be an attractive potential target for treatment of psychiatric disorders.
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