Objective: Taohong Siwu decoction (THSWD) is one of the classic prescriptions for promoting blood circulation and removing blood stasis, and it has a good therapeutic effect on ischemic stroke. We sought to explore the therapeutic effects of THSWD on pyroptosis in rats with middle cerebral artery occlusion-reperfusion (MCAO/R).Methods: MCAO/R model of rats were established by suture-occluded method. MCAO/R rats were randomly divided into five groups, which were model group, nimodipine group, THSWD high, medium and low dose group (18, 9, and 4.5 g/kg, respectively), rats of sham group without thread embolus. All rats were treated by intragastric administration for 7 days. We detected the level of inflammatory factors. NLRP3 and Caspase-1 were detected by immunofluorescence. Western blot was used to detect NLRP3, Caspase-1, ASC, and GSDMD in penumbra. Also, the expression of TXNIP, HMGB1, toll-like receptors (TLR4), NF-κB, and MAPK were detected.Results: THSWD treatment improved the behavioral function and brain pathological damage. These results showed that the levels of TNF-α, TGF-β, IL-2, IL-6, IL-1β, and IL-18 were significantly reduced in THSWD treatment groups. THSWD could significantly decrease the expression levels of NLRP3, Caspase-1, Caspase-1 p10, ASC, TXNIP, GSDMD, HMGB1, TLR4/NFκB, p38 MAPK, and JNK in penumbra.Conclusion: Our results showed that THSWD could reduce the activation level of NLRP3 inflammatory corpuscle, down-regulate GSDMD, and inhibit pyroptosis in MCAO/R rats. These may be affected by inhibiting HMGB1/TLR4/NFκB, MAPK signaling pathways.
Background: With rapid development in molecular biology techniques and a greater understanding of cancer pathogenesis, the growing attention has been concentrated on cancer gene therapy, with numerous articles on this topic published in recent 5 years. However, there is lacking a bibliometric analysis of research on cancer gene therapy. Therefore, the aim of the present study was to conduct a bibliometric analysis to provide the trends and frontiers of research on cancer gene therapy during 2016–2020.Methods: We utilized CiteSpace 5.7.R5 software to conduct a bibliometric analysis of publications on cancer gene therapy published during 2016–2020. The bibliometric records were obtained from the Web of Science Core Collection.Results: A total of 4,392 papers were included in the bibliometric analysis. Materials Science and Nanoscience and Nanotechnology took an increasing part in the field of cancer gene therapy. Additionally, WANG W was the most productive author, while ZHANG Y ranked top in terms of citations. Harvard Medical School and Sichuan University ranked top in the active institutions. P NATL ACAD SCI USA was identified as the core journal in the field of cancer gene therapy. “Ovarian cancer” was found to be the latest keyword with the strongest burst. The keyword analysis suggested that the top three latest clusters were labeled “gene delivery,” “drug delivery,” and “gene therapy.” In the reference analysis, cluster#2 labeled “gene delivery” held a dominant place considering both the node volume and mean year.Conclusion: The academic attention on cancer gene therapy was growing at a dramatically high speed. Materials Science and Nanoscience and Nanotechnology might become promising impetus for the development of this field. “Gene delivery” was thought to best reflect the research frontier on cancer gene therapy. The top-cited articles on gene delivery were focused on several novel non-viral vectors due to their specialty compared with viral vectors. “Ovarian cancer” was likely to be the potential research direction. These findings would help medical workers conduct further investigations on cancer gene therapy.
Neck dissection for oral squamous-cell carcinoma (OSCC) is a clinically controversial issue and has therefore been the subject of abundant research. However, no one has performed a bibliometric study on this topic to date. The aim of this study was to assess the development of research on neck dissection for OSCC in terms of the historical evolution, current hotspots and future directions, particularly including research trends and frontiers from 2010 to 2019. Literature records related to research on neck dissection for OSCC were retrieved from the Web of Science Core Collection (WoSCC). CiteSpace was used as a tool to perform a bibliometric analysis of this topic. The survey included 2 096 papers. “Otorhinolaryngology” was the most popular research area. The most active institutions and countries were Memorial Sloan Kettering Cancer Center and the USA, respectively. Shah J.P. was the most cited author. Among the six identified “core journals”, Head & Neck ranked first. The top three trending keywords were ‘invasion’, ‘upper aerodigestive’ and ‘negative neck’. ‘D’Cruz AK (2015)’ was the most cited and the strongest burst reference in the last decade. The study evaluated the effect on survival of elective versus therapeutic neck dissection in patients with lateralized early-stage OSCC. The depth of invasion and the management of N0 OSCC were research frontiers in this field. The present study provides a comprehensive bibliometric analysis of research on neck dissection for OSCC, which will assist investigators in exploring potential research directions.
Background Oral tongue squamous cell carcinoma (OTSCC) represents oral epithelial cell damage. Myeloblastosis (MYB) is involved in OTSCC. This study tried to probe roles of MYB in OSCC with potential axis. Methods Expression of MYB and miR-130a in OTSCC was detected. Western blot analysis was utilized to determine epithelial–mesenchymal transition-related protein levels. Dual-luciferase reporter gene assay certified the target relation between miR-130a and CYLD. Moreover, xenograft tumors in nude mice were applied to confirm the in vitro experiments. Results Both MYB and miR-130a were highly expressed in OTSCC, which promoted cell growth. Meanwhile, silenced miR-130a discouraged cell development enhanced by overexpressed MYB. CYLD was poorly expressed in OTSCC and targeted by miR-130a. Additionally, MYB knockdown activated CYLD to suppress OTSCC by downregulating miR-130a. Conclusion Our experiment supported that silenced MYB suppressed OTSCC malignancy by inhibiting miR-130a and activating CYLD. This investigation may provide novel insights for OTSCC treatment.
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