更新于：2024-11-01

Prostanoid receptor x NF-κB x TNF-α

更新于：2024-11-01

基本信息

关联

项与 Prostanoid receptor x NF-κB x TNF-α 相关的药物

RPL-228

靶点

NF-κB x Prostanoid receptor x TNF-α

作用机制

NF-κB抑制剂 [+2]

在研机构-

原研机构

Rosanto Pharmaceuticals Ltd.

在研适应症-

非在研适应症

银屑病

最高研发阶段终止

首次获批国家/地区-

首次获批日期1800-01-20

RPL-208

靶点

NF-κB x Prostanoid receptor x TNF-α

作用机制

NF-κB抑制剂 [+2]

在研机构-

原研机构

Rosanto Pharmaceuticals Ltd.

在研适应症-

非在研适应症

肿瘤

最高研发阶段终止

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 Prostanoid receptor x NF-κB x TNF-α 相关的临床结果

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100 项与 Prostanoid receptor x NF-κB x TNF-α 相关的转化医学

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0 项与 Prostanoid receptor x NF-κB x TNF-α 相关的专利（医药）

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项与 Prostanoid receptor x NF-κB x TNF-α 相关的文献（医药）

2024-10-23·Journal of Agricultural and Food Chemistry

Enteromorpha prolifera Polysaccharide Alleviates Acute Alcoholic Liver Injury in C57 BL/6 Mice through the Gut–Liver Axis and NF-κB Pathway

Article

作者: Wen, Chengrong ; Zhang, Yuying ; Yang, Jingfeng ; Yan, Tingting ; Sun, Jinghe

Enteromorpha prolifera polysaccharide (EP2) protection against acute alcoholic liver injury (AALI) in mice was investigated. By integration of physiological indicators, gut microbiota, and short-chain fatty acids (SCFAs), the mechanism of EP2 in alleviating AALI was disclosed. The results showed that EP2 significantly ameliorated alcohol-induced abnormal transaminase activities, liver and intestinal systemic inflammation, and intestinal environmental disorders. EP2 significantly reduces liver and serum LPS contents by 1.69-fold and 1.54-fold. Furthermore, inhibition of the NF-κB signaling pathway by EP2 reduced the production of proinflammatory cytokines such as TNF-α (1.83-fold), IL-6 (11.09-fold), and IL-1β (1.99-fold). EP2 restored SCFAs to normal levels by upregulating the abundance of beneficial bacteria (Colidextribacter, Ruminococcus, unclassified_Lachnospiraceae, and Akkermansia). The alleviation of AALI by EP2 occurs through protection of the intestinal mucosal barrier and reduction of LPS permeating in serum. The decrease in LPS inactivates the NF-κB signaling pathway and prevents inflammation. In short, EP2 regulates the gut-liver axis and inflammation, alleviating effects in AALI mice.

2023-11-01·Biomedicine & Pharmacotherapy

A new approach for the treatment of bleomycin-induced rat pulmonary injury by combined protein fraction of major royal jelly protein 2 and its isoform X1

Article

作者: Shaban, Nadia Z ; Abu-Serie, Marwa M ; Olleak, Shaimaa A ; Habashy, Noha H

Nowadays, royal jelly (RJ) has gained great interest as a functional food due to its valuable pharmacological effects. We investigated the therapeutic potency of combined protein fraction (PF₅₀) of major RJ protein 2 and its isoform X1 on bleomycin (Bleo)-induced pulmonary injury in rats. Our study examined the impact of PF₅₀ on pulmonary oxidative and inflammatory stress as well as smooth muscle alpha-actin (α-SMA). In addition, the predicted impacts of this PF on the activity of matrix metalloproteinase (MMP)- 8 and 15-prostaglandin dehydrogenase (15-PGDH) and the E-type prostanoid 2 (EP2) and IL-13 α2 subunit (IL13α2R) receptors, were evaluated using molecular docking. The results showed that PF₅₀ reduced pulmonary inflammatory cells and their secreted pro-inflammatory mediators, including NF-κB, IKK, IL-4, IL-6, and NO. Additionally, the levels of IgE and mucin were diminished after treatment with PF₅₀. Moreover, PF₅₀ treatment improved pulmonary oxidative stress indices such as lipid peroxidation, GSH, SOD, and GPX. The histopathological findings, chest conventional X-ray, and immunohistochemistry of α-SMA confirmed the ameliorating effect of PF₅₀. The docking outcomes reported the probable competitive inhibitory influence of PF₅₀ on MMP-8 and a postulated blocking effect on EP2 and IL13α2R. Thus, PF₅₀ could be a novel approach for treating pulmonary injuries.

2021-11-01·Molecular Immunology3区 · 医学

Live S. aureus and heat-killed S. aureus induce different inflammation-associated factors in bovine endometrial tissue in vitro

3区 · 医学

Article

作者: Li, Tingting ; Liu, Kun ; Liu, Bo ; Cao, Jinshan ; Pei, Le ; Mao, Wei ; Shen, Yuan ; Wu, Jindi ; Fu, Changqi

Staphylococcus aureus is majorly involved in bovine mastitis; however, it weakly induces pro-inflammatory factors in mammary gland epithelial cells. We aimed to clarify the involvement of S. aureus in other inflammation types and its relationship with inflammatory factor secretion in bovine endometritis. We used live S. aureus (LSA)- and heat-killed S. aureus (HK-SA)-treated bovine endometrial tissue in vitro. The HK-SA-treated group showed significantly higher IL-6, IL-1β, TNF-α, CXCL1/2 and TLR2 expression than the LSA-infected group. Contrastingly, the LSA-infected group showed significantly higher PTGS2, mPGES-1, and EP4 expression than the HK-SA treated group. There was no significant between-group difference in hyaluronan-binding protein 1 expression, which suggested similar inflammatory responses. H&E results indicated that LSA and HK-SA induced shedding of endometrial gland epithelial cells. The LSA-infected group showed higher high-mobility group box 1 protein expression than the HK-SA treated groups, which indicated differences in signaling pathway activation. Further, the LSA-treated group had higher JNK and p38 MAPK levels while the HK-SA-treated group had higher IκB-α levels. There was no significant between-group difference in the ERK signaling pathway. Our findings indicate that the pathogen-associated molecular patterns (PAMPs) of S. aureus activate pro-inflammatory factor expression via the TLR2-ERK-NF-κB signaling pathway. Contrastingly, LSA induced PGE₂ accumulation via the TLR2/MAPKs signaling pathway. This is the first report that S. aureus and the PAMPs of S. aureus activate different signaling pathways and that LSA mainly induce PGE₂ accumulation rather than cytokine secretion.