TLR4 overexpression

Furthermore, SCU was revealed to suppress OS cell proliferation by targeting TLR4 in vitro and in vivo. SCU exhibited a dual impact by inhibiting TLR4 expression and disrupting TLR4-TRAF6 interaction, resulting in NF-κB inactivation, thereby blocking OS growth.

Protective effects of Dioscin against LPS-induced SIC are achieved via regulation of TLR4/MyD88/p65 signal pathway.

ARG may reverse the resistance of human leukemia cell line K562/A02 to ADM by inhibiting TLR4/NF-κB signaling pathway.

The overexpression of TLR4 in macrophages and the close association between TLR4 and immune cell infiltration also underline the critical role of TLR4 in building the immune microenvironment for kidney cancer. These results may offer insights into the mechanism and immune microenvironment of kidney cancer.

Overexpression of TLR4 could partially reverse the effect of miR mimics on IL-1β-induced apoptosis and inflammation of OA chondrocytes. miR-515-5p negatively regulates the expression of TLR4, inhibits the activation of MyD88/NF-κB pathway and apoptosis of OA chondrocytes, and effectively alleviates the inflammatory response of the cells.

In addition, TLR4 overexpression was an independent prognostic indicator of DFS (HR= 1.480, 95%CI= 1.028- 2.130, p= 0.035) in breast cancer patients, but not related to OS(HR=1.730, 95%CI= 0.979-3.057, P= 0.059). From our main analysis results, high TLR4 expression is associated with lymph node metastasis, larger tumor size (≥2 cm), later clinical stage, negative PR expression and shorter DFS, suggesting poor prognosis in breast cancer patients.

Furthermore, it was observed that LY294002 diminished the cytoprotective effects of BB on cell injury, TLR4 expression and NF-κB activation. These findings indicated that BB could attenuate LPS-induced inflammatory injury to HepG2 cells by regulating TLR4-NF-κB signaling.

These findings suggest that Mor may ameliorate LPS-induced inflammatory damage and apoptosis in IPE through inhibition of TLR4/JAK2/STAT3 pathway.

FA inhibits U937 cell proliferation and promotes cell apoptosis by inhibiting the TLR4/NF-κB signaling pathway.

Warm ischemia in a porcine solitary kidney induces acute overexpression of TLR4 in peripheral blood leukocytes which is detectable. Relative TLR4 expression level strongly correlated with sCr, but had an observable change sooner than change in sCr. Pending further investigation, TLR4 overexpression during renal ischemia may represent a sensitive, quantitative marker of unilateral renal injury sustained during nephron-sparing surgery.

5-Fluorouracil (5-FU) is a commonly used chemotherapeutic agent for various cancers...Xenograft mouse models were established using HepG2/5-FU cells, and KGM was demonstrated to reverse 5-FU resistance in HCC tumors in vivo by suppressing TLR4 to enhance ER stress and activate PERK/ATF4/CHOP signaling. In conclusion, KGM combined with 5-FU treatment significantly promoted apoptosis and reduced cell proliferation, migration and ER stress in 5-FU-resistant HCC cells compared with KGM or 5-FU treatment alone by downregulating TLR4 to activate PERK/ATF4/CHOP signaling.

In summary, Zhigancao Decoction, a traditional Chinese medicine preparation, improves doxorubicin-inducedmyocardial apoptosis by modulating proinflammatory cytokines expression via the miRNA-21 / TLR4 / MAPK pathway. Chemotherapy, Doxorubicin, Chemotherapy toxicity, Anthracycline