Delving into the Latest Updates on 中国医科大学 with Synapse

概览

疾病领域	数量

肿瘤	1

排名前五的药物类型	数量

小分子化药	1

关联

1

项与中国医科大学相关的药物

8-Methoxyflindersine

靶点-

作用机制-

在研机构

中国医科大学

原研机构

中国医科大学

在研适应症

结直肠癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期-

100 项与中国医科大学相关的临床结果

登录后查看更多信息

0 项与中国医科大学相关的专利（医药）

登录后查看更多信息

3,518

项与中国医科大学相关的文献（医药）

2024-12-31·Journal of Oral Microbiology

P. gingivalis alters lung microbiota and aggravates disease severity of COPD rats by up-regulating Hsp90α/MLKL

Article

作者: Peng, Da ; Feng, Nan ; Han, Xuan ; Geng, Fengxue ; Wang, Hongyan ; Pan, Chunlin ; Tan, Lisi ; Pan, Yaping ; Li, Qian

BackgroundEpidemiological evidence has confirmed that periodontitis is an essential and independent risk factor of chronic obstructive pulmonary disease (COPD). Porphyromonas gingivalis, a major pathogen implicated in periodontitis, may make a vital contribution to COPD progression. However, the specific effects and molecular mechanism of the link between P. gingivalis and COPD are not clear.Methods and ResultsA COPD rat model was constructed by smoke exposure combined intratracheal instillation of E. coli-LPS, then P. gingivalis was introduced into the oral cavity of COPD rats. This research observed that lower lung function, more severe alveolar damage and inflammation occurred in COPD rats with P. gingivalis group. Meanwhile, P. gingivalis/gingipains could colonize the lung tissues and be enriched in bronchoalveolar lavage fluid (BALF) of COPD rats with P. gingivalis group, along with alterations in lung microbiota. Proteomic analysis suggested that Hsp90α/MLKL-meditated necroptosis pathway was up-regulated in P. gingivalis-induced COPD aggravation, the detection of Hsp90α and MLKL in serum and lung tissue verified that Hsp90α/MLKL was up-regulated.ConclusionThese results indicate that P. gingivalis could emigrate into the lungs, alter lung microbiota and lead to aggravation of COPD, which Hsp90α/MLKL might participate in.

2024-12-31·The Aging Male

Comment on “Risk analysis of metformin use in prostate cancer: a national population-based study”

Article

作者: Lai, Shih-Wei ; Hwang, Bing-Fang ; Liao, Kuan-Fu ; Liu, Chiu-Shong

2024-12-31·Journal of Oral Microbiology

Role of ferroptosis in Porphyromonas gingivalis- induced impairment of epithelial junction

Article

作者: Liu, Jinwen ; Shi, Xiaoting ; Zhang, Shuwei ; Lu, Ze ; Li, Jiabo ; Geng, Fengxue ; Li, Qian ; Pan, Yaping

ObjectivesThis study aims to clarify the effect of ferroptosis by P. gingivalis on periodontal epithelium impairment and potential mechanisms.Materials and methodsThe expression of epithelial junction proteins (CDH1, OCLN, ZO-1), FTL and GPX4 in healthy and periodontitis tissues was analyzed using bioinformatics analysis and validated in vivo. An in vitro model was constructed to evaluate ferroptosis by mitochondria morphology, content of iron and GSH, and level of lipid peroxidation, FTL, GPX4 and SLC7A11. The iron concentration was changed with iron chelator DFO and iron supplementation FAC. The epithelial impairment was assessed by protein expression. To investigate the mechanism, si-MYB (a negative transcription factor of SLC7A11) and GPX4 inhibitor RSL3 were employed.ResultsCDH1, OCLN, ZO-1 and GPX4 expression was decreased, while FTL expression was elevated in periodontitis tissues. Infected cells showed ferroptosis change of the mitochondria with higher level of lipid peroxidation, iron, FTL and lower level of GPX4, GSH, SLC7A11. FAC augmented ferroptosis and weakened epithelial junction, while DFO exhibited a counteractive effect. Silencing MYB rescued SLC7A11, GPX4 and epithelial junction proteins, which was hindered by RSL3.ConclusionsOur study demonstrated that P. gingivalis weakened the oral epithelial barrier by causing ferroptosis via inhibiting SLC7A11/GSH/GPX4 axis.

100 项与中国医科大学相关的药物交易

登录后查看更多信息

100 项与中国医科大学相关的转化医学

登录后查看更多信息