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      • SCIESCOPUSKCI등재

        Effects of Fengliao-Changweikang in Diarrheapredominant Irritable Bowel Syndrome Rats and Its Mechanism Involving Colonic Motility

        ( Mengdi Jia ),( Xiaofang Lu ),( Zhengfang Wang ),( Luqing Zhao ),( Shengsheng Zhang ) 대한소화기기능성질환·운동학회(구 대한소화관운동학회) 2018 Journal of Neurogastroenterology and Motility (JNM Vol.24 No.3

        Background/Aims This study was designed to investigate the effect of Fengliao-Changweikang (FLCWK) in diarrhea-predominant irritable bowel syndrome (IBS-D) rats and explore its underlying mechanisms. Methods IBS-D model rats were induced by neonatal maternal separation (NMS) combined with restraint stress (RS). In in vivo experiments, the model rats were randomly divided into 5 groups: NMS + RS, FLCWK (low dose, middle dose, and high dose), and pinaverium bromide. The normal control (no handling) rats were classified as the NH group. The therapeutic effect of FLCWK was evaluated by fecal characteristics, electromyographic response and abdominal withdrawal reflex scores. In in vitro experiments, the model rats were randomly divided into 2 groups: NMS + RS, FLCWK (middle dose), and no handling rats were used as the NH group. The differences in basic tension and ACh-induced tension of isolated colonic longitudinal smooth muscle strips (CLSMs) among the 3 groups were observed. In addition, different inhibitors (nifedipine, TMB-8, L-NAME, methylene blue, and 4-AP) were pretreated to explore the underlying mechanisms. Results In in vivo experiments, fecal characteristics, electromyographic response, and abdominal withdrawal reflex scores significantly improved in the FLCWK group, compared with the NMS + RS group. In in vitro experiments, the basic tension and ACh-induced tension of CLSMs in IBS-D rats were significantly inhibited by FLCWK. After pre-treatment with different inhibitors, the ACh-induced tension of CLSMs in each group showed no significant difference. Conclusions FLCWK manifested curative effect in IBS-D rats by inhibiting colonic contraction. The underlying mechanisms may be related to regulatory pathway of nitric oxide/cGMP/Ca<sup>2+</sup> and specific potassium channels. (J Neurogastroenterol Motil 2018;24:479-489)

      • KCI등재

        RhGLP-1 (7-36) protects diabetic rats against cerebral ischemia-reperfusion injury via up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD

        Yi Fang,Xiaofang Liu,Libo Zhao,Zhongna Wei,Daoli Jiang,Hua Shao,Yannan Zang,Jia Xu,Qian Wang,Yang Liu,Ye Peng,Xiaoxing Yin 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.5

        The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, 40 μg/kg i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7- 36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7-36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7-36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.

      • KCI등재

        An approach to automatic boundary segmentation of solid models using virtual topology: toward reconstruction of design features

        Yingzhong Zhang,Yufei Fu,Jia Jia,Xiaofang Luo 한국CDE학회 2020 Journal of computational design and engineering Vol.7 No.3

        Boundary segmentation of solid models is the geometric foundation to reconstruct design features. In this paper, based on the shape evolution analysis for the feature-based modeling process, a novel approach to the automatic boundary segmentation of solid models for reconstructing design features is proposed. The presented approach simulates the designer’s decomposing thinking on how to decompose an existing boundary representation model into a set of design features. First, the modeling traces of design features are formally represented as a set of feature vertex adjacent graphs that use low-dimensional vertex entities and their connection relations. Then, a set of Boolean segmentation loops is searched and extracted from the constructed feature vertex adjacent graphs, which segment the boundary of a solid model into a set of regions with different design feature semantics. In the search process, virtual topology operations are employed to simulate the topological changes resulting from Boolean operations in feature modeling processes. In addition, to realize effective search, search strategies and search algorithms are presented. The segmentation experiments and case study show that the presented approach is feasible and effective for the boundary segmentation of medium-level complex part models. The presented approach lays the foundation for the later reconstruction of design features.

      • SCIESCOPUSKCI등재

        RhGLP-1 (7-36) protects diabetic rats against cerebral ischemia-reperfusion injury via up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD

        Fang, Yi,Liu, Xiaofang,Zhao, Libo,Wei, Zhongna,Jiang, Daoli,Shao, Hua,Zang, Yannan,Xu, Jia,Wang, Qian,Liu, Yang,Peng, Ye,Yin, Xiaoxing The Korean Society of Pharmacology 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.5

        The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, $40{\mu}g/kg$ i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7-36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7-36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7-36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.

      • KCI등재

        Effects of strain on the optical and magnetic properties of Ce-doped ZnO

        Zhenchao Xu,Qingyu Hou,Feng Guo,Xiaofang Jia,Cong Li,Wenling Li 한국물리학회 2018 Current Applied Physics Vol.18 No.12

        The magnetic and optical properties of Ce-doped ZnO systems have been widely demonstrated, but the effects of different strains of Ce-doped ZnO systems remain unclear. To solve these problems, this study identified the effects of biaxial strain on the electronic structure, absorption spectrum, and magnetic properties of Ce-doped ZnO systems by using a generalized gradient approximation + U (GGA + U) method with plane wave pseudopotential. Under unstrained conditions, the formation energy decreased, the system became stable, and the doping process became easy with the increase in the distances between two Ce atoms. The band gap of the systems with different strains became narrower than that of undoped ZnO without strain, and the absorption spectra showed a red shift. The band gap narrowed, and the red shift became weak with the increase of compressive strain. By contrast, the band gap widened, and the red shift became significant with the increase of tensile strain. The red shift was significant when the tensile strain was 3%. The systems with −1%, 0%, and 1% strains were ferromagnetic. For the first time, the magnetic moment of the system with −1% strain was found to be the largest, and the system showed the greatest beneficial value for diluted magnetic semiconductors. The systems with −3%, −2%, 2%, and 3% strains were non-magnetic, and they had no value for diluted magnetic semiconductors. The ferromagnetism of the system with −1% strain was mainly caused by the hybrid coupling of Ce-4f, Ce-5d, and O-2p orbits. This finding was consistent with Zener's Ruderman–Kittel–Kasuya–Yosida theory. The results can serve as a reference for the design and preparation of new diluted magnetic semiconductors and optical functional materials.

      • KCI등재

        FOXK1 regulates epithelial-mesenchymal transition and radiation sensitivity in nasopharyngeal carcinoma via the JAK/STAT3 signaling pathway

        Duan Liqun,Huang Jinlong,Zhang Yong,Pi Guoliang,Ying Xiaofang,Zeng Fanyu,Hu Desheng,Ma Jia 한국유전학회 2023 Genes & Genomics Vol.45 No.6

        Background Nasopharyngeal carcinoma (NPC) is the most common head and neck tumor in China. Forkhead box (FOX) proteins have 19 subfamilies, which can maintain cell metabolism, regulate cell cycle and cell growth, etc. FOXK1 is a member of the FOX family, and studies have found that FOXK1 is closely related to tumors. Objective This experiment aims to study the effects of FOXK1 interference on proliferation, apoptosis, invasion, epithelial-mesenchymal transition (EMT), and radiosensitivity, by regulating the Janus kinas/signal translator and activator of the transfer 3 (JAK/STAT3) pathway. Methods The expression of FOXK1 was detected via immunohistochemistry using clinical nasopharyngeal carcinoma tissues and adjacent tissues. The relationship between FOXK1 expression and tumor stage was subsequently evaluated. The colony formation rate was calculated through the colony formation experiment. Cell apoptosis and cell cycle distribution were detected using flow cytometry, while cell invasion was detected using the Transwell method. The number of cells in the nucleus of each group after 30 min, 4 h, and 24 h of radiotherapy with the 2 Gy dose was counted using immunofluorescence under γ-H2AX focal points of a laser confocal microscope. Results FOXK1 is clearly expressed in the patients’ cancer tissues. The expression of FOXK1 was significantly correlated with the patient’s sex. FOXK1 interference or Peficitinib can upregulate the apoptosis rate of 5-8 F and CNE-2 cells; increase the G2 phase of cells; and inhibit the invasion, migration, and EMT of cells. At the same time, FOXK1 interference can downregulate the protein expression of p-JAK1, p-JAK2, and p-STAT3 in cells. Interference from FOXK1 or Peficitinib alone can reduce the rate of cell colony formation under different radiation doses, and enhance the green fluorescence intensity of γ-H2AX in the nucleus after 4 and 24 h of the 2 Gy dose of radiotherapy. These results are optimal when FOXK1 interference and Peficitinib are used together. Conclusion FOXK1 interference in NPC cells can regulate EMT through the JAK/STAT3 signal pathway, enhance the radiosensitivity of cells, and thus inhibit tumor cell progression.

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