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Gong S, Zhang J, Guo Z, Fu W. Drug Des Devel Ther. 2018;12:1865–1879. The Editor and Publisher of Drug Design, Development and Therapy wish to retract the published article. Concerns were raised regarding the alleged duplication of flow cytometry images in Figures 3A, 4E, 7C and 9E. The authors responded to our queries but were unable to provide a satisfactory explanation for the alleged duplication nor were they able to provide the original flow cytometry data for their study. The Editor determined the results of the study were invalid and requested for the article to be retracted. The authors agreed with this decision. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper

Fu G, Wang H, Cai Y, Zhao H, Fu W. Drug Des Devel Ther. 2018;12:1609–1619. The Editor and Publisher of Drug Design, Development and Therapy wish to retract the published article. Concerns were raised regarding the alleged duplication of western blot bands in Figure 3D. The authors explained that an error had been made by the journal which led to the unintended duplication of the Caspase-1 and IL-1β bands in Figure 3D. The journal accepts an error was made, however further investigation found the authors were unable to provide adequate original western blot data and could no longer verify the validity of the reporting findings. The decision was made to retract the article and the authors do not agree with this. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper

En Liang,1 Xiaojun Li,2 Wenjun Fu,2 Changtong Zhao,1 Baoying Yang,3 Zhonghua Yang2 1Department of Neurosurgery, The Affiliated Hexian Memorial Hospital of Southern Medical University, Guangzhou, People’s Republic of China; 2Centre for Integrative Medicine, School of Basic Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 3Department of Neurosurgery, Guangdong Sanjiu Brain Hospital, Guangzhou, People’s Republic of ChinaCorrespondence: Baoying YangDepartment of Neurosurgery, Guangdong Sanjiu Brain Hospital, No. 578 Shatai Nan Road, Baiyun District, Guangzhou, 510510, People’s Republic of ChinaEmail yby7899@163.comZhonghua YangCentre for Integrative Medicine, School of Basic Medical Science, Guangzhou University of Chinese Medicine, No. 232 Waihuan Dong Road, Panyun District, Guangzhou, 510006, People’s Republic of ChinaEmail yangzhonghua@gzucm.edu.cnBackground: The suppressor of cytokine signaling 3 (SOCS3) is a specific negative regulator of signal transducer and activator of transcription 3 (STAT3) signaling, which is predominantly activated to induce neuroinflammatory response in microglia and functions essential roles during cerebral ischemia-reperfusion (I/R) injury. Constitutive photomorphogenesis 9 (COP9) signalosome (CSN) is a signaling platform controlling protein stability by remodeling of cullin-RING ubiquitin ligases, which is recently reported to specifically recognize proteins with SOCS-box domains. However, whether SOCS3 is related to COP9 signalosome in neuroinflammation during cerebral I/R injury is completely unclear.Methods: Mice subjected to transient middle cerebral artery occlusion (MCAO) and reperfusion, and BV2 microglia cells treated with oxygen-glucose deprivation and reoxygenation (OGD/R) were used to mimic cerebral I/R injury. Western blot, qRTPCR, immunofluorescence, and co-Immunoprecipitation assays were performed to explore the regulatory me

This paper aims to construct structure-preserving numerical schemes for multi-dimensional space fractional Klein-Gordon-Schr\"{o}dinger equation, which are based on the newly developed partitioned averaged vector field methods. First, we derive an equivalent equation, and reformulate the equation as a canonical Hamiltonian system by virtue of the variational derivative of the functional with fractional Laplacian. Then, we develop a semi-discrete conservative scheme via using the Fourier pseudo-spectral method to discrete the equation in space direction. Further applying the partitioned averaged vector field methods on the temporal direction gives a class of fully-discrete schemes that can preserve the mass and energy exactly. Numerical examples are provided to confirm our theoretical analysis results at last., Comment: 26 pages, 13 figures

This paper has been retracted.Shenglan Gong,1 Jin Zhang,2 Zhouke Guo,3 Wenjun Fu1 1South China Research Center for Acupuncture and Moxibustion, School of Basic Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, People’s Republic of China; 2Department of Anatomy, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, People’s Republic of China; 3Department of Neurology and Psychology, Shenzhen Affiliated Hospital of Guangzhou University of Chinese Medicine, Shenzhen, Guangdong 518033, People’s Republic of China Background: Depression is characterized by a pathological injury to the hippocampal neurons. Senkyunolide A (SenA) is one of the major active components of Dan-zhi-xiao-yao-san, which is widely used in the treatment of depression-related disorders.Materials and methods: In the present study, it was hypothesized that the antidepressant effect of Dan-zhi-xiao-yao-san depended on the function of SenA and the authors attempted to reveal the molecular mechanism associated with the treatment. An in vitro depression model was induced using corticosterone (Cort), and the effect of SenA on the cell viability, apoptosis, and protein phosphatase 2A/α-synuclein (PP2A/α-syn) signaling was detected. To validate the mechanism driving the therapeutic effect of SenA, activity of PP2A and α-syn was modulated and the effect on neural cells was evaluated.Results: The results showed that SenA protects Cort-induced cell apoptosis in PC12 cells. In addition, SenA increased Cort-induced reduction of PP2A activity, while it decreased the expression of p-PP2A, α-syn, and p-α-syn (Ser129). Further, modulation of PP2A activity with specific inhibitor okadaic acid (OA) increased Cort-induced cell apoptosis, while PP2A activator D-erythro-sphingosine (SPH) exhibited an opposite effect. The neuroprotective effects of SenA on neural cells also depended on inhib

This paper has been retracted.Guanglei Fu,1 Hua Wang,2 Youli Cai,2 Hui Zhao,2 Wenjun Fu2 1Department of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, People’s Republic of China; 2School of Basic Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China Objective: Intracerebral hemorrhage (ICH) is one of the most common acute cerebrovascular diseases with high mortality. Numerous studies have shown that inflammatory response played an important role in ICH-induced brain injury. Theaflavin (TF) extracted from black tea has various biological functions including anti-inflammatory activity. In this study, we investigated whether TF could inhibit ICH-induced inflammatory response in rats and explored its mechanism.Materials and methods: ICH rat models were induced with type VII collagenase and pretreated with TF by gavage in different doses (25 mg/kg–100 mg/kg). Twenty-four hours after ICH attack, we evaluated the rats’ behavioral performance, the blood–brain barrier (BBB) integrity, and the formation of cerebral edema. The levels of reactive oxygen species (ROS) and inflammatory cytokines were examined by 2',7'-dichlorofluorescin diacetate and enzyme-linked immunosorbent assay. Nissl staining and transferase dUTP nick end labeling (TUNEL) were aimed to detect the neuron loss and apoptosis, the mechanism of which was explored by Western blot.Results: It was found that in the pretreated ICH rats TF significantly alleviated the behavioral defects, protected BBB integrity, and decreased the formation of cerebral edema and the levels of ROS as well as inflammatory cytokines (including interleukin-1 beta [IL-1β], IL-18, tumor nectosis factor-alpha, interferon-γ, transforming growth factor beta, and (C-X-C motif) ligand 1 [CXCL1]). Nissl staining and TUNEL displayed TF could protect against the neuron loss and apoptosis via inhibiting