scholarly journals Anti-inflammatory Effects of 8α-hydroxy pinoresinol isolated from Nardostachys jatamansi on Lipopolysaccharide-induced Inflammatory Response in RAW 264.7 Cells.

2016 ◽  
Vol 31 (5) ◽  
pp. 1-6
Author(s):  
Sun Bok Choi ◽  
Sung-Joo Park
2016 ◽  
Vol 38 (5) ◽  
pp. 1614-1620 ◽  
Author(s):  
Byoung-Man Kang ◽  
Byoung-Kwan An ◽  
Won-Seok Jung ◽  
Ho-Kyung Jung ◽  
Jung-Hee Cho ◽  
...  

2014 ◽  
Vol 29 (6) ◽  
pp. 21-26 ◽  
Author(s):  
Min-Jun Kim ◽  
Gi-Sang Bae ◽  
Sun Bok Choi ◽  
Il-Joo Jo ◽  
Dong-Goo Kim ◽  
...  

2020 ◽  
Vol 21 (23) ◽  
pp. 9283
Author(s):  
Mijin Kwon ◽  
Jaehoon Lee ◽  
Sangkyu Park ◽  
Oh-Hee Kwon ◽  
Jeongmin Seo ◽  
...  

Inflammation is a biological response of the immune system to defend the body from negative stimulation. However, the excessive inflammatory response can damage host tissues and pose serious threats. Exopolysaccharide (EPS), one of the postbiotics, is secreted from lactic acid bacteria. Although many studies have described the beneficial effects of EPS, such as its anti-inflammatory and anti-oxidant effects, its underlying mechanisms have remained to be poorly understood. Thus, we identified that EPS obtained from Lactobacillus plantarum L-14 was a homogeneous polysaccharide primarily comprised of glucose. To examine these anti-inflammatory effects, an inflammatory response was induced by lipopolysaccharide (LPS) administration to mouse macrophage RAW 264.7 cells that were pretreated with EPS. The anti-inflammatory effects of EPS were identified by analyzing the changes within inflammatory markers at the molecular level. We demonstrate here that EPS suppressed proinflammatory mediators, such as cyclooxygenase-2, interleukin-6, tumor necrosis factor-α, and interleukin-1β, and downregulated the expression of an inducible nitric oxide synthase known to lead to oxidative stress. It was also confirmed that EPS had anti-inflammatory effects by blocking the interaction of LPS with Toll-like receptor 4 (TLR4), as demonstrated by using the known TLR4 inhibitor TAK-242. In addition, we found that EPS itself could suppress the expression of TLR4. Consequently, our data suggest that EPS can be a potential target for the development of natural product-derived medicine for treating inflammatory diseases related to TLR4.


2020 ◽  
Vol 26 (38) ◽  
pp. 4934-4943
Author(s):  
Mit Joshi ◽  
Neetinkumar D. Reddy ◽  
Nitesh Kumar ◽  
Suhani Sumalatha ◽  
Mallikarjuna Rao Chamallamudi

Background: Histone deacetylase (HDAC) inhibition has been found to be effective in the treatment of inflammatory bowel disease. Previous studies have reported that Cinnamyl sulfonamide hydroxamate derivatives possess non-selective HDAC inhibition. Objective: The present study was designed to screen three selected Cinnamyl sulfonamide hydroxamate derivatives, NMJ-1, NMJ-2, and NMJ3, for in vitro anti-inflammatory response by assessing the expression of pNF-κB in lipopolysaccharide (LPS)-induced inflammatory changes on RAW 264.7 cells, and in vivo anti-inflammatory response in acetic acid (AA) and 2.4-dinitrochlorobenzene (DNCB)-induced colitis models in Wistar rats. Method: AA-induced colitis was produced in Wistar rats by intra-colonic administration of 1 ml AA. DNCBinduced colitis was produced by spraying 250 μL DNCB in acetone (20g/L) on the nape of the rats for 14 days, followed by the intracolonic administration on day 15. Drugs were administered for three days after the induction of colitis. Results: In vitro anti-inflammatory effect was observed by NMJ1 and NMJ2 through a significant decrease in pNF-κB overexpression-induced by LPS. Similar effect was observed in anti-colitis response by NMJ2 in both models by reversing the colitis-induced changes in length, weight, anti-oxidant profile and histopathology of the colon. Conclusion: NMJ2 was found to be most effective among the tested compounds as an anti-inflammatory agent in both in vitro and in vivo inflammatory studies.


2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Man-li Zhang ◽  
Hui Chen ◽  
Zhan Yang ◽  
Man-na Zhang ◽  
Xia Wang ◽  
...  

Excessive release of cytokines such as IL-1β and other inflammatory mediators synthesized and secreted by macrophages is the fundamental link of uncontrolled inflammatory response in sepsis. 17β-Estradiol (E2) plays anti-inflammatory and vascular protective effects by regulating leukocyte infiltration and the expression of chemokines or cytokines induced by injury. However, the role of E2 in the inflammatory response of macrophages in sepsis and its mechanism are still not fully understood. In the present study, we show that E2 alleviates vascular inflammation in sepsis mice induced by cecal ligation puncture (CLP). E2 significantly decreases RAW 264.7 cell inflammation response by downregulating the expression of NLRP3. Furthermore, we found that miR-29a-5p was significantly downregulated in LPS-treated macrophages. Treating RAW 264.7 cells with E2 markedly upregulated the miR-29a-5p expression level. More importantly, we demonstrated that miR-29a-5p repressed NLRP3 expression by directly targeting its 3 ′ -UTR. Loss- and gain-of-function experiments revealed that transfection of the miR-29a-5p mimic abrogates LPS-induced macrophage inflammation. Moreover, depletion of miR-29a-5p by its inhibitor largely promotes LPS-induced macrophage inflammation. In summary, miR-29a-5p upregulation induced by E2 alleviated RAW 264.7 cell inflammation response by aggravating miR-29a-5p repression of NLRP3 expression. E2 exerts significant anti-inflammatory efficacy in macrophages by regulating the miR-29a-5p/NLRP3 axis. Targeting miR-29a-5p may be a novel therapeutic strategy to suppress sepsis-induced vascular inflammation.


2013 ◽  
Vol 28 (2) ◽  
pp. 67-73 ◽  
Author(s):  
Sun-Bok Choi ◽  
Gi-Sang Bae ◽  
Il-Joo Jo ◽  
Kyoung-Chel Park ◽  
Seung-Hee Seo ◽  
...  

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