Publications by authors named "Yan Xia Tian"

Acute spontaneous intracerebral hemorrhage (ICH) is a life-threatening disease. It is often accompanied by severe neurological sequelae largely caused by the loss of integrity of the neural circuits. However, these neurological sequelae have few strong medical interventions.

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Multiple chromosome aberrations are responsible for tumorigenesis of esophagus squamous cell carcinoma (ESCC). To characterize genetic alterations by comparative genomic hybridization (CGH) and their relation to ESCC, We enrolled 54 members with ESCC from Kazakh's patients. We found that the deletions of 3p (P = 0.

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Pulmonary fibrosis (PF) is a chronic lung disease. The transforming growth factor-β1 (TGF-β1)/Smad3 signaling pathway plays an important role in the pathogenesis of pulmonary fibrosis. Bone marrow-derived mesenchymal stem cells (BMSCs) have been shown to be a modulator of the molecular aspects of the fibrosis pathway.

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The aim of the present study was to evaluate the effects of bone marrow-derived mesenchymal stem cells (BMSCs) on the expression of the autophagy-associated proteins, microtubule-associated protein light chain 3 (LC-3) and autophagy-related gene Beclin-1 (Beclin-1), in alveolar macrophages (AMs) in a rat model of silicosis. Furthermore, the study investigated the molecular mechanisms underlying the effects of BMSC treatment. A population of 60 adult female Sprague-Dawley (SD) rats were allocated at random into three groups, namely the control, model and BMSC treatment groups (n=20 per group).

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  • Traumatic brain injury (TBI) causes delayed neuronal dysfunction and long-term cognitive issues, and effective treatments are still being sought.
  • A study tested whether resveratrol (100 mg/kg) can improve recovery in rats with TBI, finding it reduced brain swelling and improved cognitive function and neurological performance.
  • Resveratrol treatment boosted the expression of certain synaptic proteins and decreased markers of neuronal autophagy, suggesting its potential as a new therapy for TBI.
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Previous research has demonstrated that traumatic brain injury (TBI) activates autophagy and a neuroinflammatory cascade that contributes to substantial neuronal damage and behavioral impairment, and Toll-like receptor 4 (TLR4) is an important mediator of this cascade. In the present study, we investigated the hypothesis that resveratrol (RV), a natural polyphenolic compound with potent multifaceted properties, alleviates brain damage mediated by TLR4 following TBI. Adult male Sprague Dawley rats, subjected to controlled cortical impact (CCI) injury, were intraperitoneally injected with RV (100 mg/kg, daily for 3 days) after the onset of TBI.

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  • Rhein lysinate (RHL) effectively inhibits the growth of various tumor cells, including those from breast and ovarian cancers, as well as glioma cells in xenograft models.
  • In studies using U87 glioma cells, RHL treatment led to a significant reduction in cell proliferation and tumor growth in mice, highlighting its potential as an antitumor agent.
  • The mechanism behind RHL's effectiveness involves increased production of reactive oxygen species (ROS) and apoptosis, along with changes in key proteins regulating cell survival and the cell cycle.
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The P2X7 inhibitor, brilliant blue G (BBG), has been reported as a neuroprotective drug against a variety of disorders, including neuropathic pain and brain ischemia. Currently, no studies have examined the potential for BBG to provide neuroprotection in animal models of TBI. The aim of the present study was to investigate the neuroprotective effect of BBG on TBI and to determine the underlying mechanisms.

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  • Chloroquine (CQ) has shown potential as an autophagy inhibitor and was investigated for neuroprotective effects in traumatic brain injury (TBI) models.
  • The study involved administering CQ to rats immediately post-injury and assessing its impact on brain edema and functional deficits using various tests.
  • Results indicated that CQ treatment reduced brain edema and improved motor and cognitive functions by suppressing neuronal autophagy and inflammatory cytokine levels in the hippocampus.
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Connexins, gap junction proteins, have short half‑lives of only a few hours; therefore, degradation of these proteins can rapidly modulate their function. Autophagy is a type of degradation pathway that has been implicated in several diseases and was reported to be induced following traumatic brain injury (TBI). The aim of the present study was to investigate the involvement of neuronic autophagy in proteolysis of phosphorylated connexin 43 (p‑Cx43) in hippocampal astrocytes following TBI in rats.

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  • Gap junctions, made of connexin proteins, facilitate the exchange of small molecules and ions between cells and have been linked to autophagy activation after traumatic brain injury (TBI).
  • In a study using Sprague-Dawley rats, researchers found that levels of phosphorylated connexin 43 (p-CX43) peaked 6 hours post-injury and were located in astrocytes near pyramidal neurons, while LC3-II levels were sustained high for 24 hours.
  • The inhibition of p-CX43 led to decreased autophagy, indicating that gap junctions play a pivotal role in regulating autophagy in hippocampal neurons following TBI.
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Silicosis is a well-known occupational disease, characterized by epithelial injury, fibroblast proliferation, expansion of the lung matrix and dyspnea. At present, no effective treatment methods for silicosis have been identified. The present study aimed to investigate the protective potential of exogenous bone marrow-derived mesenchymal stem cell (BMSC) transplantation on experimental silica-induced pulmonary fibrosis in rats and analyze the underlying paracrine mechanisms associated with its therapeutic effects.

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  • Diffuse brain injury (DBI) is a significant cause of death and disability in young people and adults, leading to long-term cognitive and motor impairments.
  • The study examines how the NADPH oxidase (NOX) complex, particularly the NOX2 protein, is activated following DBI in rats, contributing to additional brain damage.
  • Results show that inhibiting NOX activity with apocynin reduces brain damage and enhances spatial learning, suggesting a potential neuroprotective treatment for DBI.
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Background: Activation of c-Jun NH(2)-terminal kinase (JNK) has been implicated in neuron apoptosis as well as autophagy in response to various stressors after traumatic brain injury (TBI). However, the underlying molecular pathway remains unclear. Our study assessed whether JNK-mediated p53 phosphorylation might be an important mechanism for enhancing neuron autophagy in response to TBI.

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Objective: To study the effect and potential mechanism of expression of c-jun N-terminal kinase (JNK) signal pathway on neuron autophagy after diffuse brain injury (DBI).

Methods: Male Sprague Dawley rats (n = 216) were randomly divided into four groups: DBI group (n = 54), SP600125 intervene group (n = 54), DMSO group (n = 54) and sham operation group (n = 54). DBI rat model was established according to the description of Marmarou DBI.

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  • The study investigates the protective effects of edaravone on severe traumatic brain injury (TBI) in rats, aiming to understand its underlying mechanisms.
  • Two hundred and seventy-three male rats were divided into four groups: control, model (TBI), low-dose, and high-dose edaravone treatment, with various assessments made on brain tissue damage and neuron apoptosis over time.
  • Results indicated that edaravone treatment reduced neuronal damage, apoptosis, and improved learning and memory function compared to untreated TBI rats, suggesting a therapeutic potential for edaravone in TBI recovery.
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Objective: To explore the effect of N-acetyl L-cysteine (NAC) on expressions of matrix metalloproteinases-2, 9 (MMP-2, MMP-9) in lung fibroblasts of SiO(2) exposed rats.

Methods: Seventy-five Wistar rats were divided randomly into three groups. The control group was administered with normal Saline.

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