Aucubin ameliorates the LPS‐induced inflammatory response in bovine endometrial epithelial cells by inhibiting NF‐κB and activating the Keap1/Nrf2 signaling pathway

2021 ◽  
Author(s):  
Feng Gao ◽  
Huatao Li ◽  
Yanni Feng ◽  
Wenru Tian ◽  
Rongfeng Cao ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Nrf2 Signaling Pathway ◽  
Endometrial Epithelial Cells

scholarly journals ISGylation Inhibits an LPS-Induced Inflammatory Response via the TLR4/NF-κB Signaling Pathway in Goat Endometrial Epithelial Cells

Animals ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 2593
Author(s):  
Jinbang Xiao ◽  
Shanshan Li ◽  
Ruixue Zhang ◽  
Zongjie Wang ◽  
Xinyan Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Potential Method ◽  
Modification System ◽  
Disease Etiology ◽  
Principal Factors ◽  
Reproductive Disease ◽  
Endometrial Epithelial Cells

Endometritis is a common and important reproductive disease of domestic animals. The principal factors responsible for the disease are infection with Gram-negative bacteria, the release of Lipopolysaccharides (LPS) and activation of the TLR4/NF-κB signaling pathway. However, we do not fully understand the interaction between endometrial immunity and bacterial infection in the disease etiology. The ubiquitin-like protein ISG15 can regulate the TLR4/NF-κB signaling pathway via the ISGylation modification system, modulating the inflammatory response. In the present study, we found that ISG15 protein was expressed mainly in the cytoplasm of goat endometrial epithelial cells (gEECs) and that the expression of key genes and proteins of ISGylation increased in LPS-induced gEECs. Overexpression and silencing of the ISG15 gene demonstrated that ISGylation inhibited an LPS-induced inflammatory response via the TLR4/NF-κB signaling pathway in gEECs. Here, we provide the experimental basis for further exploration of the role of the ISGylation modification system in the inflammatory response of endometrium and a potential method for the treatment of endometritis.

Polydatin inhibits the IL-1β-induced inflammatory response in human osteoarthritic chondrocytes by activating the Nrf2 signaling pathway and ameliorates murine osteoarthritis

2018 ◽  
Vol 9 (3) ◽  
pp. 1701-1712 ◽  
Author(s):  
Shangkun Tang ◽  
Qian Tang ◽  
Jialei Jin ◽  
Gang Zheng ◽  
Jianchen Xu ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Osteoarthritic Chondrocytes ◽  
Nrf2 Signaling Pathway ◽  
Prevalent Form

Osteoarthritis (OA), which is characterized by progressive degradation of the articular cartilage, is the most prevalent form of human arthritis.

Treatment of Intrauterine Adhesions with Human Amnion Mesenchymal Stromal Cells (hAMSCs) on Promoting Endometrial Regeneration and Repair Via Notch Signaling Pathway Regulation

2020 ◽  
Author(s):  
Jie Yu ◽  
Wenwen Zhang ◽  
Jiayue Huang ◽  
Yating Gou ◽  
Congcong Sun ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Intrauterine Adhesions ◽  
Epithelial Markers ◽  
Qrt Pcr ◽  
Endometrial Epithelial Cells

Abstract Background: Human amniotic mesenchymal stem cells(hAMSCs) can repair and improve the damaged endometrium which its aplastic disorder is the main reason for intrauterine adhesions(IUAs).Methods: We conducted in vivo and in vitro experiments. In vivo experiments: 45 female Sprague-Dawley(SD) rats were involved and randomized equally into Sham group, IUA group, Estradiol(E2) group, hAMSCs group, and E2 + hAMSCs group. The effect of hAMSCs and E2 only or combined was evaluated by Hematoxylin-eosin(HE) and Masson staining. The expression of epithelial markers and key proteins of Notch signaling pathway by Immunohistochemistry. In vitro experiments: Firstly, the hAMSCs cells were taken and divided into control group and induced group in which hAMSCs were differentiated into endometrial epithelial cells in induced microenvironment, and extracted their RNA respectively. The expression of epithelial markers and Notch1 messenger RNA (mRNA) was detected by Real-time quantitative polymerase chain reaction(qRT-PCR). and the changes in expression position of Notch intracellular domain(NICD) and expression amount of target gene, hairy enhancer of split 1(Hes1) were detected by Immunofluorescence. Then, Activated and inhibited the Notch signaling pathway while induction, and detected mRNA expression of hAMSCs epithelial markers by quantitative real-time polymerase chainreaction (qRT-PCR) respectively and detected hAMSCs cell cycle by flow cytometric. Results:This study showed that hAMSCs alone or combined with E2 could promote endometrial repair, and Notch signaling pathway a great role in it. And otherwise, the activation or habitation of Notch signaling pathway determines whether hAMSCs could differentiate into endometrial epithelial cells or not.Conclusion: we concluded that activate the Notch signaling pathway promote the differentiation of hAMSCs into endometrial epithelial cells, and further treat IUAs.

scholarly journals Anti-Inflammatory Effects of Neochlorogenic Acid Extract from Mulberry Leaf (Morus alba L.) Against LPS-Stimulated Inflammatory Response through Mediating the AMPK/Nrf2 Signaling Pathway in A549 Cells

Molecules ◽  
2020 ◽  
Vol 25 (6) ◽  
pp. 1385 ◽  
Author(s):  
Xiao-han Gao ◽  
Sun-dong Zhang ◽  
Li-tao Wang ◽  
Liang Yu ◽  
Xue-lian Zhao ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
A549 Cells ◽  
Morus Alba ◽  
Mulberry Leaf ◽  
Tnf Α ◽  
Nrf2 Signaling Pathway ◽  
Acute Pneumonia ◽  
Neochlorogenic Acid ◽  
Anti Inflammatory

Neochlorogenic acid (nCGA) is a phenolic compound isolated from mulberry leaf (Morus alba L.), which possesses multiple pharmacological activities containing antioxidant and anti-inflammatory effects. However, the role of nCGA in the treatment of acute pneumonia and the underlying molecular mechanism are still unclear. Hence, the aim of study is to investigate the anti-inflammatory properties of nCGA on LPS-stimulated inflammation in A549 cells. In the present study, results reported that nCGA without cytotoxicity significantly reduced the production of TNF-α, IL-6, and NO, and further suppressed the proteins of iNOS, COX2, TNF-α, IL-6 expression. Furthermore, nCGA also inhibited NF-κB activation and blocked MAPKs signaling pathway phosphorylation. In addition, we found nCGA significantly increased the expression of HO-1 via activating the AMPK/Nrf2 signaling pathway to attenuate the inflammatory response, whereas this protective effect of nCGA was reversed by pre-treatment with compound C (C.C, an AMPK inhibitor). Therefore, all these results indicated that nCGA might act as a natural anti-inflammatory agent for the treatment of acute pneumonia.

Sign in / Sign up

Export Citation Format

Share Document