Molecular medicine reports最新文献

Following the publication of the above paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Fig. 1C and D on p. 2386 were strikingly similar to data appearing in different form in a pair of other articles written by different authors at a different research institute that had already been published elsewhere prior to the submission of this paper to Molecular Medicine Reports. Moreover, some of the data featured in Fig. 6A and C were strikingly similar, also suggesting that the data in this figure had been misassembled. In view of the fact that the abovementioned data had already apparently been published previously, the Editor of Molecular Medicine Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 2384‑2392, 2018; DOI: 10.3892/mmr.2017.8152].

Endometriosis (EM) is a chronic inflammatory disease that is one of the most common causes of gynecological systemic lesions in women before menopause. The most representative histological feature of EM is that the endometrium appears outside of the uterine cavity, often in the ovary. Although it is generally accepted that the epithelial and stromal cells of the ectopic endometrium are not malignant, they still have numerous similarities to malignant tumors, including considerable changes to the immune microenvironment (immune monitoring disorder), the creation of a specific hormone environment, high levels of oxidative stress, chronic inflammation and abnormal immune cell regulation. The pathogenesis of EM is not fully understood, which makes it difficult to identify specific biomarkers and potential therapeutic targets for early disease diagnosis and effective treatment. However, considerable progress has been made in this field over the past few decades. The purpose of the present review is to summarize the confirmed and potential biomarkers for EM, and to identify potential therapeutic targets based on changes in immunological factors (including natural killer cells, macrophages, the complement system, miRNA and P‑selectin) in the ectopic endometrial tissue. It is hoped that this work can be used as the basis for identifying accurate diagnostic markers for EM and developing personalized immune‑targeted therapy.

Osteoarthritis (OA) is a common joint disorder involving the cartilage and other joint tissues. Quercetin (QCT) serves a protective role in the development of OA. However, to the best of our knowledge, the regulatory mechanisms of QCT in the progression of OA have not yet been fully elucidated. In order to mimic a model of OA in vitro, IL‑1β was used to stimulate chondrocytes. Furthermore, an in vivo animal model of OA was induced by anterior cruciate ligament transection (ACLT). 5‑Ethynyl‑2'‑deoxyuridine assays, TUNEL assays, ELISAs, western blotting and immunohistochemical assays were conducted to assess the chondroprotective properties of QCT in the development of OA. The results revealed that 100 µM QCT significantly promoted the proliferation, reduced the apoptosis and inflammation, and inhibited the extracellular matrix (ECM) degradation in IL‑1β‑stimulated chondrocytes. Additionally, QCT attenuated the IL‑1β‑induced ferroptosis of chondrocytes, as demonstrated by the reduced lipid reactive oxygen species and Fe²⁺ levels. Conversely, the inhibitory effects of QCT on the apoptosis and inflammatory responses were reversed by the activation of ferroptosis by erastin in IL‑1β‑stimulated chondrocytes. Furthermore, QCT significantly elevated the level of phosphorylated (p‑)5' AMP‑activated protein kinase (AMPK) and the levels of two negative regulators of ferroptosis [nuclear factor erythroid 2‑related factor 2 (Nrf2) and glutathione peroxidase 4 (Gpx4)] in IL‑1β‑stimulated chondrocytes. The AMPK inhibitor compound C notably reversed the promoting effects of QCT on phosphorylated‑AMPK, Nrf2 and Gpx4 expression in IL‑1β‑stimulated chondrocytes. Additionally, QCT markedly ameliorated the destruction and degradation of articular cartilage, and elevated the p‑AMPK, Nrf2 and Gpx4 levels in the mouse model of ACLT‑induced OA. Overall, the present study demonstrated that QCT inhibited the development of OA by suppressing ferroptosis via the activation of the AMPK/Nrf2/Gpx4 signaling pathway. These findings provide novel insights into the regulatory mechanisms of QCT for the treatment of patients with OA.

Among patients with chronic epilepsy, 70‑80% have cognitive impairment. To investigate the relationship between adiponectin (ADPN) and the cognitive level in epilepsy and its mechanism, 20 epileptic patients and 20 healthy controls were included for the assessment of the cognitive level. An ELISA was used to evaluate the serum ADPN level. An epileptic rat model was established and treated with AdipoRon, an ADPN receptor (AdipoR) agonist, which binds to AdipoR1 and AdipoR2. The Morris water maze test was used to assess the cognitive function of rats, and the expression levels of the synapsis‑associated proteins postsynaptic density protein 95 (PSD95), synaptosomal associated protein 25 (SNAP25) and synaptophysin (SYP), as well as AMP‑activated protein kinase (AMPK), mTOR, phosphorylated (p‑)AMPK and p‑mTOR were determined by immunoblotting. Serum ADPN levels were positively correlated with the Montreal cognitive assessment score. AdipoRon improved the cognitive function of epileptic rats, maintained the structural integrity of hippocampal neurons and reduced neuronal damage. It also promoted the mRNA expression of AdipoR1 and AdipoR2 in the hippocampus. Furthermore, AdipoRon increased the expression of the synapsis‑associated proteins PSD95, SNAP25 and SYP by activating the AMPK/mTOR signaling pathway. ADPN improved cognitive impairment in epilepsy by targeting the AMPK/mTOR signaling pathway, providing novel insights for the treatment of epilepsy.

Subarachnoid hemorrhage (SAH), a prevalent cerebrovascular condition associated with a high mortality rate, frequently results in neuronal apoptosis and an unfavorable prognosis. The adjunctive use of traditional Chinese medicine (TCM) with surgical interventions exerts a therapeutic impact on SAH, potentially by facilitating apoptosis. However, the mechanism by which TCM mediates apoptosis following SAH remains unclear. In the present study, C57BL/6J mice were subjected to the modified single‑clamp puncture method to produce an in vivo model of SAH. Treatment of these mice with notoginsenoside R1 (NGR1) prevented short‑term neurological deficits, reduced the expression levels of apoptosis‑associated proteins and mitigated brain edema. In addition, an in vitro model of SAH was established by treating HT22 mouse neuronal cells with oxyhemoglobin (OxyHb). Treatment of these cells with NGR1 resulted in attenuation of the OxyHb‑induced apoptosis. Furthermore, RNA sequencing analysis was used to examine NGR1 + OxyHb and OxyHb groups. Statistically significant changes in the expression levels of apoptosis‑associated genes in OxyHb‑stimulated HT22 cells upon administration of NGR1 were observed. The present study investigated the potential mechanism by which NGR1 mitigates neuronal apoptosis, presenting a novel therapeutic approach for treating SAH through the use of a single TCM component.

Ischemic stroke is a prevalent clinical condition that poses a significant global challenge. Developing innovative strategies to address this issue is crucial. Annexin A1 (ANXA1), a key member of the annexin superfamily, performs various functions, such as inhibiting inflammatory factor release, promoting phagocytosis, and blocking leukocyte migration. Evidence indicates that ANXA1 plays a pivotal role in the pathogenesis of ischemic stroke. The present article reviews involvement of ANXA1 in anti‑atherosclerosis, inflammatory processes, blood‑brain barrier protection, platelet aggregation and anti‑apoptotic mechanisms. The potential applications of ANXA1 in treating ischemic stroke are also explored.

Most psychiatric disorders are heterogeneous and are attributed to the synergistic action of a multitude of factors. It is generally accepted that psychiatric disorders are the outcome of interactions between genetic predisposition and environmental perturbations, which involve psychosocial stress, or alterations in the physiological state of the organism. A number of hypotheses have been presented on such environmental influences that may include direct insults such as injury, malnutrition and hostile living conditions, or indirect sequelae following infection from viruses such as influenza, arboviruses, enteroviruses and several herpesviruses, or the differential expression of human endogenous retroviruses. It is known that the concept of viruses is far more extensive than their perception as mere agents of acute infections, or chronic debilitating diseases, such as AIDS or some forms of cancer. Notably, an apparent causal connection between viruses and the pathophysiology of diseases has been suggested; however, it remains unclear as to how to establish this causal connection. There are inherent difficulties in answering this question with certainty, which may be due to the multitude of genetic and environmental influences that can lead to psychopathology; the latent state of chronic infection exhibited by a number of neurotropic viruses; the late onset of psychiatric disorders with respect to the acute phase of viral infection at which detection tests would be successful; the complexity of the virome; and the existence of thousands of viral species. The present review aims to provide an outline of the conclusions that have thus far been reached regarding a possible association between viral infection and psychiatric disease, and the obstacles confronted during the quest for the truth behind the role of viruses.

Aseptic loosening (AL) of artificial hip joints is the most common complication following hip replacement surgery. A total of eight patients diagnosed with AL following total hip arthroplasty (THA) undergoing total hip replacement and eight control patients diagnosed with avascular necrosis of femoral head (ANFH) or femoral neck fracture undergoing THA were enrolled. The samples of the AL group were from synovial tissue surrounding the lining/head/neck of the prosthesis, and the samples of the control group were from the synovium in the joint cavity. The present study utilized second‑generation high‑throughput sequencing and mass spectrometry to detect differentially expressed genes, proteins and metabolites in the samples, as well as Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. Key genes cytokine receptor‑like factor‑1 (CRLF1) and glutathione‑S transferase µ1 (GSTM1) expression levels were verified by reverse transcription‑quantitative PCR and western blotting. The integrated transcriptomics, proteomics and untargeted metabolomics analyses revealed characteristic metabolite changes (biosynthesis of guanine, L‑glycine and adenosine) and decreased CRLF1 and GSTM1 in AL, which were primarily associated with amino acid metabolism and lipid metabolism. In summary, the present study may uncover the underlying mechanisms of AL pathology and provide stable and accurate biomarkers for early warning and diagnosis.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the IL‑1 protein data shown in the western blotting data in Fig. 5A on p. 1905, the hippocampal images shown in Fig. 6A and certain of the immunohistochemical data shown in Fig. 6B on p. 1906 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to Molecular Medicine Reports, or were under consideration for publication at around the same time. In view of the fact that certain of the abovementioned data had already apparently been published previously, the Editor of Molecular Medicine Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 1899‑1908, 2018; DOI: 10.3892/mmr.2018.9227].