Xiaodong Peng

Capital Medical University

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Nian Liu

Beijing Anzhen Hospital

Xuesi Wang

Beijing Anzhen Hospital

Xinmeng Liu

Tianjin University

Changsheng Ma

Beijing Anzhen Hospital

Rong Lin

Fuzhou University

Yanfei Ruan

Beijing Anzhen Hospital

Donald L. Durden

University of California, San Diego

Jianzeng Dong

First Affiliated Hospital of Zhengzhou University

Yukun Li

Zhuzhou Central Hospital

Linling Li

Wuhan Polytechnic University

Cooperative Institutions

Capital Medical University

Beijing Anzhen Hospital

Sichuan University

Indiana University – Purdue University Indianapolis

National Clinical Research Center for Digestive Diseases

Ningxia Medical University

Indiana University School of Medicine

Chinese Academy of Sciences

Shanghai Jiao Tong University

National Clinical Research

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[Hypnotic effect of Chinese materia medica Cynanchum chinese in mice].

PubMed (2007)

Xiaodong Peng Yan QianShun Rui Wang Weidong Yang Peng Jian-zhong

To study the central pharmacological effect of the water and chloroform-extract compounds from C. chinese in mice.The independent activity test and the hypnotic synergism test by sub-threshold hypnotic dosage of pentobarbital were employed to evaluate the central pharmacological effect of the extract-compounds, and the minimal neurotoxicity was evaluated by the rotorod test.the extract-compounds exhibited significant dose-related inhibition effect of the spontaneous motor activity in mice after intraperitoneal administration. And the two extract-compounds promoted the hypnotic effect by sub-threshold hypnotic dosage administration of pentobarbital, and produced ED50 value of 2.36 g kg (-1) and 0.75 g kg(-1), respectively. Also, both extract-compounds showed no neurotoxicity in the experiment.The extract compounds from C. chinese showed inhibitional effect on CNS.

ED50

Neurotoxicity

Intraperitoneal injection

Locomotor activity

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RAC mediated phagocytosis and the activation of - receptor γ SHP-1 regulates Fc

Anita Kant Pradip De Xiaodong Peng Taolin Yi David J. Rawlings

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Neuropharmacological insight into preventive intervention in posttraumatic epilepsy based on regulating glutamate homeostasis

CNS Neuroscience & Therapeutics (2023)

Yuan Gao Ning Liu Juan Chen Ping Zheng Jianguo Niu

Abstract Background Posttraumatic epilepsy (PTE) is one of the most critical complications of traumatic brain injury (TBI), significantly increasing TBI patients' neuropsychiatric symptoms and mortality. The abnormal accumulation of glutamate caused by TBI and its secondary excitotoxicity are essential reasons for neural network reorganization and functional neural plasticity changes, contributing to the occurrence and development of PTE. Restoring glutamate balance in the early stage of TBI is expected to play a neuroprotective role and reduce the risk of PTE. Aims To provide a neuropharmacological insight for drug development to prevent PTE based on regulating glutamate homeostasis. Methods We discussed how TBI affects glutamate homeostasis and its relationship with PTE. Furthermore, we also summarized the research progress of molecular pathways for regulating glutamate homeostasis after TBI and pharmacological studies aim to prevent PTE by restoring glutamate balance. Results TBI can lead to the accumulation of glutamate in the brain, which increases the risk of PTE. Targeting the molecular pathways affecting glutamate homeostasis helps restore normal glutamate levels and is neuroprotective. Discussion Taking glutamate homeostasis regulation as a means for new drug development can avoid the side effects caused by direct inhibition of glutamate receptors, expecting to alleviate the diseases related to abnormal glutamate levels in the brain, such as PTE, Parkinson's disease, depression, and cognitive impairment. Conclusion It is a promising strategy to regulate glutamate homeostasis through pharmacological methods after TBI, thereby decreasing nerve injury and preventing PTE.

Excitotoxicity

Homeostasis

10.1111/cns.14294

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Visualization and mapping of the right phrenic nerve by intracardiac echocardiography during atrial fibrillation ablation

EP Europace (2023)

Xinmeng Liu Rong Lin Xiaodong Peng Xuesi Wang Yukun Li

This study aimed to evaluate the feasibility of real-time visualization and mapping of the right phrenic nerve (RPN) by using intracardiac echocardiography (ICE) during atrial fibrillation (AF) ablation.RPN injury is a complication associated with the ablation of AF. Multiple approaches are currently being used to prevent and detect RPN injuries. However, none of these approaches can directly visualize the RPN in real-time during the ablation procedure.The RPN was detected using ICE. The RPN and its adjacent structures were analysed. The relationship between the RPN's distance from the superior vena cava (SVC) and its pacing capture threshold was quantified. The safety of SVC isolation guided by the ICE-visualized RPN was evaluated. Thirty-eight people were enrolled in this study. The RPN was visualized by ICE in 92% of patients. It ran through the space between the SVC and the mediastinal pleura and had a 'straw'-like appearance upon ICE imaging. The course of the RPN was close to the SVC (minimum 1.0 ± 0.4 mm) and the right superior pulmonary vein (minimum 14.1 ± 7.3 mm). There was a positive linear correlation between the RPN's capture threshold and its distance from the SVC (Spearman's correlation coefficient = 0.728, < 0.001). SVC isolation was guided by the RPN; none of the patients developed an RPN injury.RPN can be visualized by ICE in most patients, thus providing a novel approach for the real-time detection of RPN during AF ablation.

10.1093/europace/euad012

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Phrenic Nerve Injury During Ablation of Atrial Fibrillation: Mechanisms, Clinical Features, Prognosis, and Prevention Methods

Cardiovascular Innovations and Applications (2023)

Xinmeng Liu Rong Lin Xiaodong Peng Xuesi Wang Yukun Li

Atrial fibrillation ablation procedures have become a focus of research among electrophysiologists, with the aim of increasing success rates while minimizing complications. One major concern is phrenic nerve injury (PNI). Despite advancements in ablation strategies, equipment, and monitoring methods, the incidence of PNI during these procedures remains substantial, particularly during cryoballoon ablation, which has a reported PNI incidence of 3.5%. This review examines recent studies, to provide a comprehensive overview of PNI mechanisms, clinical features, prognosis, and methods for prevention during ablation.

Phrenic nerve

10.15212/cvia.2023.0050

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Neuroprotective strategies for neonatal hypoxic-ischemic brain damage: Current status and challenges

European Journal of Pharmacology (2023)

Qing You Xiaobing Lan Ning Liu Juan Du Lin Ma

Brain damage

10.1016/j.ejphar.2023.176003

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Exploring a structural protein-drug interactome for new therapeutics in lung cancer

PMC (2014)

Xiaodong Peng Fang Wang Liwei Li Khuchtumur Bum‐Erdene David Xu

Interactome

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CCL2 influences the sensitivity of lung cancer A549 cells to docetaxel

Oncology Letters (2018)

Ting Wang Qingyuan Zhan Xiaodong Peng Zhimin Qiu Tiantian Zhao

Lung cancer is one of the most common malignant tumor types globally. Acquisition of chemoresistance in lung cancer cells is the primary cause of chemotherapy failure. Inflammatory chemokine C‑C motif chemokine ligand 2 (CCL2) has been reported to be involved in the progression of cancer and drug resistance. However, its function in docetaxel (DTX) resistance of lung cancer remains unclear. In the present study, the mechanism underlying DTX‑induced drug resistance was investigated. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis revealed that DTX treatment increased the mRNA and protein expression of CCL2 in lung cancer A549 cells. CCL2 was knocked down by small interfering RNA or was overexpressed by recombinant CCL2 lentivirus, and cell viability was determined. An MTT assay indicated that CCL2 downregulation decreased the viability of A549 cells and augmented the DTX‑induced cytotoxicity, whereas CCL2 upregulation protected A549 cells from DTX‑induced cytotoxicity. Additionally, it was revealed that CCL2 overexpression activated phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling and inhibited apoptosis‑associated protein caspase‑3 activation and B‑cell lymphoma 2 (Bcl‑2) phosphorylation at Ser70 induced by DTX, and enhanced DTX‑induced Bcl‑2‑associated death promoter phosphorylation at Ser112. PI3K/AKT inhibitor LY294002 restored DTX‑induced caspase‑3 activation and Bcl‑2 phosphorylation, reversed the effect of CCL2 on the viability of A549 cells and enhanced DTX‑induced cytotoxicity. These results demonstrated that chemoresistance may be mediated by cell stress responses involving CCL2 expression, suggesting that CCL2 may be a potential target for enhancing the therapeutic effect of DTX in lung cancer.

Viability assay

MTT assay

10.3892/ol.2018.8769

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Rap1a Null Mice Have Altered Myeloid Cell Functions Suggesting Distinct Roles for the Closely Related Rap1a and 1b Proteins

The Journal of Immunology (2007)

Yu Li Jingliang Yan Pradip De Hua-Chen Chang Akira Yamauchi

Abstract The Ras-related GTPases Rap1a and 1b have been implicated in multiple biological events including cell adhesion, free radical production, and cancer. To gain a better understanding of Rap1 function in mammalian physiology, we deleted the Rap1a gene. Although loss of Rap1a expression did not initially affect mouse size or viability, upon backcross into C57BL/6J mice some Rap1a−/− embryos died in utero. T cell, B cell, or myeloid cell development was not disrupted in Rap1a −/− mice. However, macrophages from Rap1a null mice exhibited increased haptotaxis on fibronectin and vitronectin matrices that correlated with decreased adhesion. Chemotaxis of lymphoid and myeloid cells in response to CXCL12 or CCL21 was significantly reduced. In contrast, an increase in FcR-mediated phagocytosis was observed. Because Rap1a was previously copurified with the human neutrophil NADPH oxidase, we addressed whether GTPase loss affected superoxide production. Neutrophils from Rap1a−/− mice had reduced fMLP-stimulated superoxide production as well as a weaker initial response to phorbol ester. These results suggest that, despite 95% amino acid sequence identity, similar intracellular distribution, and broad tissue distribution, Rap1a and 1b are not functionally redundant but rather differentially regulate certain cellular events.

10.4049/jimmunol.179.12.8322

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Prevalence and risk factors of thyroid carcinoma

Guoji zhongliuxue zazhi (2014)

Lingzhi Cao Jianping Xie Xiaodong Peng

The incidence of thyroid carcinoma is associated with a variety of factors.Radiation is the clear risk factor,the relationship between iodine intake and thyroid carcinoma remains controversial.Researches show that the genetic and epigenetic changes of many signaling pathways are the key of molecular pathogenetic mechanism of thyroid carcinoma.In addition,thyroid stimulating hormone,body mass index and chronic lymphocytic thyroiditis are also associated with thyroid carcinoma. Key words: Thyroid neoplasms ; Incidence ; Risk factors

10.3760/cma.j.issn.1673-422x.2014.04.009

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