PTGS2 expression

A COX inhibitor aspirin potently increases the antitumor effects of IFN-α in the suppression of HCC cell proliferation in vivo. Higher expression of COX2 and phosphorylated STAT3 is associated with poor development and prognosis in HCC patients by analyzing human HCC clinical samples. These observations suggest that a fundamental PKA/SHP2-dependent negative feedback loop acts on IFN signaling, and inhibition of this signaling by the selective COX2 inhibitors may enhance the clinical efficacy of type I IFNs in treating HCC.

IL-32θ (A94V) suppresses the expressions of COX-2, GM-CSF, and CYP1A1 by blocking the nuclear translocation of NF-κB and AP-1, as well as inhibiting the activation of the AhR/ARNT signaling pathway. Our findings offer valuable insights into developing therapeutic strategies and potential drugs to mitigate PM-induced skin inflammation by inhibiting the ERK/p38/NF-κB/AP-1 and AhR/ARNT signaling pathways.

Moreover, MITF expression was inhibited by reduced mitogen-activated protein kinase and protein kinase B phosphorylation levels. Overall, this study proves the efficacy of the novel DB-14 exosome as a strong lightening and anti-inflammatory agent.

Furthermore, IL-1β-induced elevation of inflammatory cytokines, PTGS2 protein expression, and phosphorylated p38/p38 ratios in chondrocytes were significantly attenuated upon WFY intervention. Our study systematically elucidated the pharmacological basis and molecular mechanism underlying WFY's therapeutic effects in KOA, substantiating its ability to suppress inflammation and regulate PTGS2 expression and p38 phosphorylation.

Jeoryeong-tang has a promising therapeutic potential for treating IBD through its anti-inflammatory properties. Findings of this study suggest that JRT could be a valuable candidate for further clinical investigations in the treatment of IBD.

Studies have shown that ALKBH3 is upregulated in most tumors, but the role of ALKBH3 in AML remains unclear. In this study, we investigated the function of ALKBH3 in AML cells (KG-1) by immunofluorescence, ELISA, flow cytometry, HE staining, and Western blotting. Our results revealed that ALKBH3 is upregulated in AML and that the downregulation of ALKBH3 inhibited KG-1 cell proliferation and promoted cell apoptosis; at the same time, ALKBH3 upregulated ATF4 expression through m1A demethylation, and the knockdown of ATF4 resulted in increased ferrous iron content; TFR1, ACSL4, and PTGS2 expression; and ROS and MDA levels, whereas SOD and GSH levels and the expression levels of ATF4, SLC7A11, GPX4, and FTH1 decreased in KG-1 cells, thereby promoting ferroptosis. Mechanistically, ALKBH3-mediated m1A demethylation suppressed ferroptosis in KG-1 cells by increasing ATF4 expression, thereby promoting the development of AML. Our study indicated that reducing the expression of ALKBH3 might be a potential target for improving AML symptoms.

Additionally, NOD1 was required in M1/M2 polarization in vivo mediated by Exos. In conclusion, CAF-secreted Exos facilitated M2 macrophage polarization by carrying PTGS2 to activate the NOD1 pathway, thereby promoting pancreatic cancer metastasis, providing evidence that CAF-Exos accelerating pancreatic cancer progression.

SNX30 inhibits lung adenocarcinoma cell proliferation and induces ferroptosis by regulating SETDB1 expression.

Clinically, altered Ptgs2 was closely associated with adverse cardiovascular outcomes. Overall, the combination of AST and 5-FU significantly enhanced cardiotoxicity by inducing cardiomyocyte apoptosis, inflammation, and the expression of Ptgs2.

The mechanisms by which MEL mitigated the inflammatory response and oxidative stress were partially attributed to inhibition of the nuclear transcription factor-kappa B (NF-κB) signaling pathway and improvement of the activation of the nuclear factor erythroid 2-related factors (Nrf2) signaling pathway. To conclude, the results manifested that MEL at plasma maintenance concentrations protected BMECs from inflammatory and oxidative damage induced by K. pneumoniae.

Msol was more effective than MS in suppressing renal IL-1β and COX-2 expressions. In summary, the findings indicate that Msol shows potential as a novel therapeutic agent for treating liver and kidney injuries associated with diabetic complications.

This research paves the way for detailed investigations on the impact of environment structural transitions on the spectral properties of fluorogenic probes. Moreover, the fact that COX-2 exists as homodimer just in cancer tissues, but as monomer elsewhere, gives novel hints for therapeutical avenues to fight cancer and contributes to the development of drugs targeted to COX-2 dimer in cancer, but without affecting constitutive COX-2, thus minimizing off-target effects.