Plantamajoside attenuates inflammatory response in LPS-stimulated human gingival fibroblasts by inhibiting PI3K/AKT signaling pathway

2019 ◽  
Vol 127 ◽  
pp. 208-211 ◽  
Author(s):  
Fei Liu ◽  
Xin Huang ◽  
Jing-jun He ◽  
Ci Song ◽  
Ling Peng ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Human Gingival Fibroblasts ◽  
Gingival Fibroblasts ◽  
Akt Signaling Pathway

scholarly journals Effect of phenytoin on PI3K/Akt signaling pathway in human gingival fibroblasts

2020 ◽  
Vol 93 (0) ◽  
pp. 1-P-083
Author(s):  
Hiroko Matsumoto ◽  
Reiri Takeuchi ◽  
Junichi Yamane ◽  
Hitoshi Nishimura ◽  
Masamichi Komiya
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Human Gingival Fibroblasts ◽  
Gingival Fibroblasts ◽  
Akt Signaling Pathway

scholarly journals Retraction: Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signaling pathway in IL-1β-induced osteoarthritis chondrocytes

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4441-4441
Author(s):  
Laura Fisher
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Akt Signaling ◽  
Salvianolic Acid B ◽  
Signalling Pathway ◽  
Akt Signaling Pathway ◽  
Salvianolic Acid ◽  
Osteoarthritis Chondrocytes

Retraction of ‘Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signalling pathway in IL-1β-induced osteoarthritis chondrocytes’ by Bin Zhu et al., RSC Adv., 2018, 8, 36422–36429, DOI: 10.1039/C8RA02418A.

scholarly journals LINC02085 Regulates Cell Growth and Inflammatory Response in Rheumatoid Arthritis by Regulating PI3K/ AKT Signaling Pathway

2020 ◽  
Author(s):  
Jianting Wen ◽  
Jian Liu ◽  
Xin Wang ◽  
Jie Wang
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Growth ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Arthritis Score ◽  
Akt Signaling Pathway ◽  
Primary Fibroblast

Abstract Background: The present study explored the possible functions and the underlying mechanism of long Non-coding RNA LINC02085 in rheumatoid arthritis (RA). Methods: Primary fibroblast-like synoviocytes (FLS) were separated from synovial tissues and was established cell lines, then cultured for subsequent cell experiments by transfecting different vectors. Rat with AA were injected with sh-LINC02085. The progression of AA was explored by measuring arthritis score and histologic analysis. ELISA analysis was employed to detect the levels of inflammatory cytokines. CCK8 assay, migration and invasion assays were used to evaluate the proliferation, migration and invasion abilities of cells, respectively. Besides, the levels of the the PI3K/AKT pathway-related proteins were measured by WB and IF. Results: The expression level of LINC02085 was significant high in patients with RA, and positively associated with clinical indexes. We found that LINC02085 was upregulated in RA -FLS and TNF-αstimulated. And overexpression of LINC02085 could promote proliferation, migration and invasion induced by TNF-α, through upregulating the levels of TNF-αand TNFAIP2 and promoting the activation of PI3K/AKT pathway. Whereas downexpression of LINC02085 received the opposite results. Knockdown of LINC02085 significantly ameliorated the progression of AA reflected by decreased arthritis score and cartilage destruction. Conclusion: The present study revealed that LINC02085 could regulate cell growth and inflammatory response of RA-FLS by activating the PI3K/ AKT signaling pathway, subsequently playing important roles in promoting the occurrence and development of RA.

scholarly journals 6-Gingerol Protects Heart by Suppressing Myocardial Ischemia/Reperfusion Induced Inflammation via the PI3K/Akt-Dependent Mechanism in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Tongtong Xu ◽  
Guowei Qin ◽  
Wei Jiang ◽  
Ying Zhao ◽  
Yongnan Xu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Inflammatory Response ◽  
Cardiac Function ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Myocardial Ischemia Reperfusion

Our previous study has demonstrated that 6-Gingerol (6-G) could alleviate myocardial ischemia/reperfusion injury (MIRI). However, the molecular mechanism underlying the process of myocardial ischemia/reperfusion (I/R) injury alleviation by 6-G remains unelucidated. The objective of the present study is to further investigate the potential mechanism for 6-G to alleviate MIRI in rats. Thirty-two Sprague-Dawley rats were randomly divided into four groups: the Sham group, the I/R group, the 6-G + I/R group, and the LY294002 (LY) + 6-G + I/R group. For the rats in each of the groups, data were collected for cardiogram, cardiac function, area of myocardial infarction, myocardial pathology, myocardial enzyme, marker of inflammatory response, and PI3K/Akt signaling pathway. We found that the pretreatment of 6-G with 6 mg/kg could shrink the ST section of cardiogram, improve the cardiac function, reduce the area of myocardial infarction and the degree of cardiac pathological injury, lower the level of myocardial enzyme, and inhibit the inflammatory response. In addition, our results also indicated that 6-G could upregulate the expression of PI3K and p-Akt and that LY294002, a blocking agent of PI3K/Akt signaling pathway, could nullify the protecting role of 6-G. Our experimental results showed that 6-G could inhibit I/R-induced inflammatory response through the activation of the PI3K/Akt signaling pathway.

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