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BACKGROUND: Targeted therapy based on nuclear transcription factor kappa B signaling pathway to explore neuroinflammation is increasingly worth exploring, and the advantages of Chinese medicine such as many targets, wide range, rich mechanisms, and few side effects have great potential in the treatment of various diseases. OBJECTIVE: Based on the nuclear transcription factor kappa B signaling pathway, this paper systematically expounded and summarized the research progress of kaempferol, safflower yellow, baicalin, and triptolide in the treatment of neuroinflammation after spinal cord injury. METHODS: Search terms “spinal cord injury, inflammation, anti-inflammatory, traditional Chinese medicine monomer, monomeric compound, NF-κB signaling pathway, flavonoids, glycosides, phenols, esters, alkaloids” were searched in CNKI and PubMed databases. Totally 67 articles were finally included. RESULTS AND CONCLUSION: (1) The role of nuclear transcription factor kappa B signaling pathway in the nervous system is complex and diverse, which can regulate neutrophils, microglia, astrocytes, and macrophages, and mediate the occurrence and development of inflammation after injury. (2) The effects of traditional Chinese medicine monomers such as baicalin on the degradation of nuclear transcription factor kappa B inhibitory protein, the inhibition of phosphorylation process by safflowerin on nuclear transcription factor kappa B signaling pathway, and the inhibition of kaempferol on nuclear transcription factor kappa B signaling pathway p65 nuclear translocation can reduce the impact of inflammatory response on the body, thereby promoting the recovery of neurological function. (3) The nuclear transcription factor kappa B signaling pathway can promote inflammation and immune cell migration and activation in the early stage of injury, and can promote the repair of injury site and the occurrence of fibrosis in the middle and late stages of injury. Appropriate activation of the nuclear transcription factor kappa B signaling pathway can promote the release of inflammatory factors, improve the antioxidant capacity of cells, and promote the activation of immune cells, but the over-activated nuclear transcription factor kappa B signaling pathway can easily lead to the occurrence and continuation of chronic inflammation and the inhibition of apoptosis. (4) Future research can further explore how to accurately regulate the activation level of nuclear transcription factor kappa B signaling pathway, how to achieve precise intervention for nervous system inflammation and injury, and can also focus on the preparation of traditional Chinese medicine monomers and the mechanism of action of traditional Chinese medicine monomers on signaling pathways, in order to provide more effective treatment strategies for the rehabilitation and functional recovery of neurological diseases. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research 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.)

Copyright of Journal of China University of Petroleum is the property of China University of Petroleum 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.)

Objective：To discuss the effect of apolipoprotein C1 (APOC1) expression on the proliferation and apoptosis of the hepatocellular carcinoma cells, and to preliminarily clarify the related molecular mechanism. Methods：The expression level of APOC1 mRNA in hepatocellular carcinoma tissue and its relationship with the prognosis of the patient were analyzed by The Cancer Genome Atlas (TCGA) Database； real-time fluorescence quantitative PCR (RT-qPCR) method was used to detect the expression levels of APOC1 mRNA in different hepatocellular carcinoma cells； the human liver cancer HepG2 cells with low APOC1 expression were selected as the subjects. The HepG2 cells were transfected with pcDNA3. 1-APOC1 plasmid to over-express APOC1（APOC1 over-expression group), and the HepG2 cells transfected with empty vector pcDNA3. 1 were regarded as control group. MTS assay and 5-ethynyl2'-deoxyuridine (EdU) staining were used to detect the proliferative activities and proliferation rates of the cells in two groups； Transwell chamber assay was used to detect the numbers of migration cells in two groups；flow cytometry and TUNEL assay were used to detect the percentages of the cells at different cell cycles and apoptotic rates in two groups；Western blotting method was used to detect the expression levels of extracellular regulated protein kinase (ERK), phosphorylated ERK (p-ERK), protein kinase B (AKT), phosphorylated AKT (p-AKT), B-cell lymphoma-2 (Bcl-2), and cleaved cysteinyl aspartate specific proteinase-3 (cleaved caspase-3) proteins in the cells in two groups. Results：The TCGA Database results showed that the expression level of APOC1 mRNA in hepatocellular carcinoma tissue was lower than that in normal liver tissue (P<0. 05), and the patients with low expression of APOC1 mRNA had poor prognosis. The RT-qPCR results showed that the expression level of APOC1 mRNA in the HepG2 cells was the lowest, and the HepG2 cells were chosen for the subsequent research. Compared with control group, the proliferative activity and proliferation rate of the cells in APOC1 over-expression group were decreased (P<0. 05 or P<0. 01), the number of migration cells was decreased (P<0. 01), and the percentage of the cells at S phase and the apoptotic rate were significantly increased (P<0. 01) . Compared with control group, the expression levels of p-ERK, p-AKT, and Bcl-2 proteins in the cells in APOC1 over-expression group were significantly decreased (P<0. 05), and the expression level of cleaved caspase-3 protein was increased (P<0. 01) . Conclusion：High expression of APOC1 can inhibit the proliferation of the human liver cancer HepG2 cells and induce the apoptosis, and its mechanism may be related to inhibition of the expressions of p-ERK, p-AKT, Bcl-2 proteins and promotion of the expression of cleaved caspase-3 protein. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research 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.)

Copyright of Science Technology & Engineering is the property of Chinese Society of Technology Economics 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.)

Copyright of Ordnance Industry Automation is the property of Editorial Board for Ordnance Industry Automation 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.)

Copyright of Special Oil & Gas Reservoirs is the property of Special Oil & Gas Reservoirs Editorial Office 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.)

Pre-eclampsia (PE) is a polygenic and multi -system damaging disease unique to the second and third trimester of pregnancy. If the disease progresses severely, it can lead to complications such as placental abruption, diffuse intravascular coagulation (DIC), eclampsia, and HELLP syndrome. It is the main cause of rising maternal and neonatal morbidity and mortality worldwide. Due to the dynamic progress of PE, and the clinical manifestations are diversified, the principle of treatment is mainly antispasmodic, antihypertensive, sedative and so on. The timely termination of pregnancy is the most effective clinical treatment. At present, studies on its etiology are still controversial. Most studies show that vascular endothelial function damage caused by immune and hormone response during pregnancy is the main pathophysiological change of PE. Among them, the inflammatory cascade caused by neutrophil activation plays an important role in the occurrence and development of PE. This article reviews the research progress on the role of neutrophil activation in vascular endothelial function damage in the pathogenesis of PE. [ABSTRACT FROM AUTHOR]

Pre-eclampsia (PE) is a pregnancy-specific idiopathic disease that causes an increase in maternal and neonatal morbidity and mortality worldwide. At present, the cause is not completely clear, and it is difficult to predict changes by a single biomarker. Termination of pregnancy is the only effective treatment for patients with PE who show no improvement or progressive deterioration after active treatment. Scholars believe that vascular endothelial cell injury is the main pathogenesis of PE. Recent studies have found that abnormal expression of tumor necrosis factor alpha (TNF-α) in plasma of PE patients is involved in the occurrence and development of the disease. Upon binding of TNF-α to related receptors, activation of the mitogen-activated protein kinase (MAPK) signaling pathway results in upregulation of the downstream target protein myeloperoxidase (MPO). The release of MPO after excessive activation of neutrophils, and its increased expression level is a key factor of vascular endothelial cell injury. To review the research progress on the mechanism of TNF-αregulating MPO in the pathogenesis of PE. [ABSTRACT FROM AUTHOR]

Copyright of Journal of China Medical University is the property of Journal of China Medical University Editorial Office 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.)

Copyright of Journal of Beijing University of Traditional Chinese Medicine is the property of Journal of Beijing University of Traditional Chinese Medicine 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.)