المؤلفون: Huang, Liaoyuan, Chen, Jianming, Wu, Danhai, Wang, Kan, Lou, Weigang, Wu, Jianmin

المصدر: BioMed Research International; 7/23/2022, p1-11, 11p

مصطلحات موضوعية: THERAPEUTIC use of alkaloids, INTERLEUKINS, SPINE diseases, STAINS & staining (Microscopy), ALKALOIDS, ANIMAL experimentation, AUTOPHAGY, INTERVERTEBRAL disk, MTOR inhibitors, SIGNAL peptides, APOPTOSIS, HEALTH outcome assessment, CELLULAR signal transduction, CELL nuclei, RATS, IMMUNOBLOTTING, CELL proliferation, FLUORESCENT antibody technique, DESCRIPTIVE statistics, PHARMACODYNAMICS

مستخلص: Intervertebral disc degeneration (IDD) is a chronic progressive condition mainly caused by excessive inflammatory cytokines. Berberine (BBR) exerts anti-inflammatory effect on diseases and protective effect against IDD. However, the mechanism is not uncertain. This study is aimed at investigating the molecular mechanism of BBR on IDD. Nucleus pulposus (NP) cells were treated with BBR at different concentrations. The IDD rat model was established by acupuncture. The effect of BBR on interleukin- (IL-) 1β-induced cell proliferation was measured by CCK-8 assay and BrdU staining. The role of BBR in IL-1β-induced apoptosis, autophagy repression, and extracellular matrix (ECM) degradation was measured by Annexin/PI staining, immunofluorescence, and immunoblot. The effect of BBR on IDD was investigated in rat. Our findings showed that BBR restored cell growth and attenuated apoptosis in IL-1β-induced NP cells. BBR also prevented the IL-1β-induced ECM degradation through regulating ECM-related enzymes and factors. Additionally, BBR significantly activated autophagy repressed by IL-1β. Autophagy stimulated by BBR was diminished by the inhibition of the AMPK/mTOR/Ulk1 signaling pathway. In vivo study also showed BBR attenuated intervertebral disc degeneration. BBR could attenuate NP cells apoptosis and ECM degradation induced by IL-1β through autophagy by the AMPK/mTOR/Ulk1 pathway. This study suggests BBR might function as an AMPK activator to alleviate IDD progression. [ABSTRACT FROM AUTHOR]

: Copyright of BioMed Research International is the property of Hindawi Limited and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Wang, Zizong, Yang, Bin, Zhang, Jin, Chu, Xiangyang

المصدر: BioMed Research International; 7/8/2022, p1-16, 16p

مصطلحات موضوعية: RNA metabolism, LUNG cancer, DISEASE progression, COMPETITIVE endogenous RNA, EXPERIMENTAL design, CELL migration, WESTERN immunoblotting, MICROBIOLOGICAL assay, MTOR inhibitors, CELLULAR signal transduction, BIOINFORMATICS, GENE expression, DESCRIPTIVE statistics, POLYMERASE chain reaction

مستخلص: Objectives. This study focused on the biological functions and mechanisms of action of LINC01554 in nonsmall cell lung cancer (NSCLC). Methods. The expression and prognostic values of LINC01554 in NSCLC were evaluated using The Cancer Genome Atlas datasets. MTT, colony formation, wound healing, transwell, and in vivo assays were performed to investigate the role of LINC01554 in NSCLC. The related protein expression levels were measured via western blotting. Bioinformatic analysis was conducted to predict targeted genes. The relationship between LINC01554, microRNA- (miR-) 1267, miR-1267, and inhibitor of growth family member 3 (ING3) was analysed via a dual-luciferase reporter assay. Results. LINC01554 expression was downregulated in NSCLC and associated with NSCLC prognosis. LINC01554 overexpression suppressed NSCLC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Bioinformatic and dual-luciferase reporter assays demonstrated that LINC01554 expression directly targeted miR-1267 expression, which in turn directly acted on ING3. An miR-1267 mimic significantly reduced ING3 expression, whereas an miR-1267 inhibitor observably elevated its expression. LINC01554 overexpression increased ING3 expression, whereas this effect was counteracted by the miR-1267 mimic. LINC01554 overexpression also significantly suppressed the expression of phosphorylated protein kinase B (Akt) and phosphorylated mammalian target of rapamycin (mTOR) expression; this effect was abrogated by the miR-1267 mimic. Mechanistically, LINC01554 overexpression repressed the growth, migration, invasion, and epithelial-mesenchymal transition (EMT) of NSCLC cells through the regulation of the miR-1267/ING3 axis via regulation of the Akt/mTOR signalling pathway. Conclusions. We provide the first evidence of the involvement of the LINC01554/miR-1267 axis in NSCLC proliferation and metastasis through the ING3Akt/mTOR pathway. Thus, LINC01554 may serve as a novel therapeutic target for NSCLC. [ABSTRACT FROM AUTHOR]

: Copyright of BioMed Research International is the property of Hindawi Limited and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Shen, Bairu, Cen, Zhuofei, Tan, Minghua, Song, Changshan, Wu, Xuhui, Wang, Jiaqing, Huang, Minqian

المصدر: BioMed Research International; 2/18/2022, p1-12, 12p

مصطلحات موضوعية: TUMOR prevention, TUMOR diagnosis, TUMOR treatment, ONLINE information services, HEART transplantation, SYSTEMATIC reviews, LUNG transplantation, KIDNEY transplantation, MTOR inhibitors, MYCOPHENOLIC acid, SKIN tumors, KAPOSI'S sarcoma, GASTROINTESTINAL tumors, LIVER diseases, MEDLINE, LIVER transplantation, TUMORS, LYMPHOPROLIFERATIVE disorders, IMMUNOSUPPRESSIVE agents, RADIATION injuries, TRANSPLANTATION of organs, tissues, etc., IMMUNOTHERAPY, DISEASE risk factors, THERAPEUTICS

مصطلحات جغرافية: UNITED States, EUROPE, ASIA

مستخلص: Objective. To analyze the diagnosis and treatment of patients with concomitant malignant tumors after organ transplantation by compiling data from organ transplantation patients. Methods. By searching CNKI and PubMed databases, we made a systematic analysis of the studies of postorgan transplantation complicating malignant tumors in the last decade. Results. There were 10 articles on malignant tumors after renal transplantation, 8 articles on liver transplantation, 2 articles on heart transplantation, and 1 article on lung transplantation. The incidence of malignant tumors complicating renal transplantation is 10.4% in Europe, with skin cancer and Kaposi's sarcoma being common; the incidence in the United States is 3.4%, with PTLD having the highest incidence; the incidence of malignant tumors is relatively lowest in Asia, with gastrointestinal malignancies being the main ones. The mean time to complication of malignancy after renal transplantation is 3.83 years. The incidence of concurrent malignancies after liver transplantation is 8.8% in Europe, where skin cancer and Kaposi's sarcoma are common; 5.6% in Asia, where gastrointestinal tract tumors are prevalent; and 4.5% in the United States, where gastrointestinal tract tumors, PTLD, and hematologic diseases are predominant. The mean time to complication of malignancy after liver transplantation is 4.79 years. The incidence of malignancy after heart transplantation is 6.8-10.7%. The incidence of malignancy after lung transplantation is about 10.1%. Minimization of immunosuppression or modification of immunosuppression regimens may be a key component of cancer prevention. mTOR inhibitors and phenolate (MMF) reduce the incidence of de novo malignancies in patients after solid organ transplantation. Surgical treatment improves survival in patients with early malignancies. The use of external beam radiation therapy in the treatment of hepatocellular carcinoma is limited due to the risk of radiation liver disease. Conclusions. The risk of concomitant malignancy needs to be guarded for 5 years of immunosuppressive therapy after organ transplantation surgery. Adjusting the immunosuppressive treatment regimen is an effective way to reduce concurrent malignancies. Systemic chemotherapy or radiotherapy requires vigilance against the toxic effects of drug metabolism kinetics on the transplanted organ. [ABSTRACT FROM AUTHOR]

: Copyright of BioMed Research International is the property of Hindawi Limited and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Lucia Lisi, Pierluigi Navarra, Paola Aceto, Cinzia Dello Russo

المصدر: BioMed Research International, Vol 2015 (2015)
BioMed Research International

مصطلحات موضوعية: AMPK, Settore BIO/14 - FARMACOLOGIA, Sensory Receptor Cells, lcsh:Medicine, Review Article, Bioinformatics, mTORC2, General Biochemistry, Genetics and Molecular Biology, Ganglia, Spinal, medicine, Animals, Humans, Pain Management, Kinase activity, mTORC1, Protein kinase B, PI3K/AKT/mTOR pathway, hyperalgesia, neuropathic pain, General Immunology and Microbiology, rapamycin, business.industry, AKT, TOR Serine-Threonine Kinases, lcsh:R, Chronic pain, General Medicine, medicine.disease, ERK, ATP-competitive mTOR inhibitors, Anesthesia, Neuropathic pain, Hyperalgesia, mTOR, Neuralgia, Chronic Pain, medicine.symptom, metformin, business, Cancer pain, mechanical allodynia

الوصف: Chronic pain represents a major public health problem worldwide. Current pharmacological treatments for chronic pain syndromes, including neuropathic pain, are only partially effective, with significant pain relief achieved in 40–60% of patients. Recent studies suggest that the mammalian target of rapamycin (mTOR) kinase and downstream effectors may be implicated in the development of chronic inflammatory, neuropathic, and cancer pain. The expression and activity of mTOR have been detected in peripheral and central regions involved in pain transmission. mTOR immunoreactivity was found in primary sensory axons, in dorsal root ganglia (DRG), and in dorsal horn neurons. This kinase is a master regulator of protein synthesis, and it is critically involved in the regulation of several neuronal functions, including the synaptic plasticity that is a major mechanism leading to the development of chronic pain. Enhanced activation of this pathway is present in different experimental models of chronic pain. Consistently, pharmacological inhibition of the kinase activity turned out to have significant antinociceptive effects in several experimental models of inflammatory and neuropathic pain. We will review the main evidence from animal and human studies supporting the hypothesis that mTOR may be a novel pharmacological target for the management of chronic pain.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e59617df233f57653da7e36a22ab1f4cTest
https://doaj.org/article/2902f715e515454c981c331f3f2ecee6Test