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- 저자 : Fanxing Xu (검색결과 4 건)
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Fanxing Xu,Bosai He,Feng Xiao,Tingxu Yan,Kaishun Bi,Ying Jia,Zhenzhong Wang 한국응용약물학회 2019 Biomolecules & Therapeutics(구 응용약물학회지) Vol.27 No.1
Previous studies have shown that spinosin was implicated in the modulation of sedation and hypnosis, while its effects on learning and memory deficits were rarely reported. The aim of this study is to investigate the effects of spinosin on the improvement of cognitive impairment in model mice with Alzheimer’s disease (AD) induced by Aβ1-42 and determine the underlying mechanism. Spontaneous locomotion assessment and Morris water maze test were performed to investigate the impact of spinosin on behavioral activities, and the pathological changes were assayed by biochemical analyses and histological assay. After 7 days of intracerebroventricular (ICV) administration of spinosin (100 μg/kg/day), the cognitive impairment of mice induced by Aβ1-42 was significantly attenuated. Moreover, spinosin treatment effectively decreased the level of malondialdehyde (MDA) and Aβ1-42 accumulation in hippocampus. Aβ1-42 induced alterations in the expression of brain derived neurotrophic factor (BDNF) and B-cell lymphoma-2 (Bcl-2), as well as inflammatory response in brain were also reversed by spinosin treatment. These results indicated that the ameliorating effect of spinosin on cognitive impairment might be mediated through the regulation of oxidative stress, inflammatory process, apoptotic program and neurotrophic factor expression,suggesting that spinosin might be beneficial to treat learning and memory deficits in patients with AD via multi-targets.
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Spinosin Inhibits Aβ<sub>1-42</sub> Production and Aggregation via Activating Nrf2/HO-1 Pathway
( Xiaoying Zhang ),( Jinyu Wang ),( Guowei Gong ),( Ruixin Ma ),( Fanxing Xu ),( Tingxu Yan ),( Bo Wu ),( Ying Jia ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.3
The present research work primarily investigated whether spinosin has the potential of improving the pathogenesis of Alzheimer’s disease (AD) driven by β-amyloid (Aβ) overproduction through impacting the procession of amyloid precursor protein (APP). Wild type mouse Neuro-2a cells (N2a/WT) and N2a stably expressing human APP695 (N2a/APP695) cells were treated with spinosin for 24 h. The levels of APP protein and secreted enzymes closely related to APP procession were examined by western blot analysis. Oxidative stress related proteins, such as nuclear factor-erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) were detected by immunofluorescence assay and western blot analysis, respectively. The intracellular reactive oxygen species (ROS) level was analyzed by flow cytometry, the levels of Aβ<sub>1-42 </sub>were determined by ELISA kit, and Thioflavin T (ThT) assay was used to detect the effect of spinosin on Aβ<sub>1-42 </sub>aggregation. The results showed that ROS induced the expression of ADAM10 and reduced the expression of BACE1, while spinosin inhibited ROS production by activating Nrf2 and up-regulating the expression of HO-1. Additionally, spinosin reduced Aβ<sub>1-42 </sub>production by impacting the procession of APP. In addition, spinosin inhibited the aggregation of Aβ<sub>1-42</sub>. In conclusion, spinosin reduced Aβ<sub>1-42</sub> production by activating the Nrf2/HO-1 pathway in N2a/WT and N2a/ APP695 cells. Therefore, spinosin is expected to be a promising treatment of AD.
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( Chun Chu ),( Xiang Gao ),( Xiang Li ),( Xiaoying Zhang ),( Ruixin Ma ),( Ying Jia ),( Dahong Li ),( Dongkai Wang ),( Fanxing Xu ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.2
Silibinin exhibits antidiabetic potential by preserving the mass and function of pancreatic β-cells through up-regulation of estrogen receptor-α (ERα) expression. However, the underlying protective mechanism of silibinin in pancreatic β-cells is still unclear. In the current study, we sought to determine whether ERα acts as the target of silibinin for the modulation of antioxidative response in pancreatic β-cells under high glucose and high fat conditions. Our in vivo study revealed that a 4-week oral administration of silibinin (100 mg/kg/day) decreased fasting blood glucose with a concurrent increase in levels of serum insulin in high-fat diet/streptozotocin- induced type 2 diabetic rats. Moreover, expression of ERα, NF-E2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) in pancreatic β-cells in pancreatic islets was increased by silibinin treatment. Accordingly, silibinin (10 μM) elevated viability, insulin biosynthesis, and insulin secretion of high glucose/palmitate-treated INS-1 cells accompanied by increased expression of ERα, Nrf2, and HO-1 as well as decreased reactive oxygen species production in vitro. Treatment using an ERα antagonist (MPP) in INS-1 cells or silencing ERα expression in INS-1 and NIT-1 cells with siRNA abolished the protective effects of silibinin. Our study suggests that silibinin activates the Nrf2-antioxidative pathways in pancreatic β-cells through regulation of ERα expression.
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Role of silibinin in the management of diabetes mellitus and its complications
Chun Chu,Da-Hong Li,Shicheng Zhang,Takashi Ikejima,Ying Jia,Dongkai Wang,Fanxing Xu 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.8
Diabetes mellitus is globally approaching epidemicproportions and acts as a major cause of a number ofserious health problems diagnosed as diabetic complications. The current oral drugs in the treatment of diabetesand its complications could meet some but not all of thepatients’ needs, and the development of novel drugs with ahypoglycemic effect is urgently required. Silibinin, aflavonolignan traditionally used for the treatment of gallbladderand hepatic diseases, was reported to improveglycemic homeostasis by improving the activity of pancreaticb-cells, increasing insulin sensitivity of liver andmuscle cells, and decreasing lipid deposition in adipocytes. Researches also indicated the effectiveness of silibinin incontrolling several diabetic complications including neuropathy,retinopathy, impaired healing, hepatopathy, cardiomyopathy,nephropathy, and osteoporosis. In thisreview, we summarize the recent anti-diabetes findings ofsilibinin and clarify the underlying pharmacologicalmechanisms, and update the knowledge in understandingthe role of silibinin in control of diabetic complications.
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