文献引用
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1) A network pharmacology approach and experimental validation to investigate the neuroprotective mechanism of quercetin against alcoholic brain injury via the JNK/P38 MAPK signaling pathway.
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2) Luteolin ameliorates kainic acid-induced seizure by modulating GADD45B and reducing oxidative stress in hippocampal neurons.
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3) Evodiamine protects against cardiac remodeling in heart failure through modulation of calcium signaling and CD47.
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4) Tyrosol ameliorates depressive-like behavior and hippocampal damage in perimenopausal depression rats by inhibiting oxidative stress and thyroid dysfunction.
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5) APOE modulates ferroptosis to drive macrophage polarization toward the M2 type and enhance PTC migration and invasion.
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6) OSW-1 inhibits tumor cell proliferation and migration via uncoupling protein 2 in hepatocellular carcinoma.
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7) MiR-4472 serves as a potential biomarker for hypoxic-ischemic encephalopathy and promotes neuronal death as well as hypoxic-ischemic brain damage in neonatal rats by targeting MEF2D.
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8) Bioinformatics analysis reveals the diagnostic and therapeutic value of the centrosome replication-related gene SPICE1 in keloid.
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9) Calycosin Protects Against Chronic Prostatitis via Regulating Cellular Pyroptosis.
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10) Alleviation of fibrosis and oxidative stress in pressure overload-induced cardiac remodeling and heart failure via SIRT3 activation by colchicine.
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11) Mitochondrial RNA/RIG-I promotes Caspase-1/GSDMD-mediated inflammation in sepsis-associated acute kidney injury.
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12) The role of quercetin in modulating lipid metabolism and enhancing chemotherapy via the STAT3-CPT1B pathway in pancreatic cancer.
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13) Guaiane sesquiterpenoid-Glucozaluzanin C from Ainsliaea fragrans Champ. targets TLR4/p65 to regulate NF-κB/MAPK pathway, alleviating sepsis-induced acute liver injury.
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14) Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviate Helicobacter pylori-associated gastritis.
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15) Cadmium exposure induces Leydig cell injury via necroptosis caused by oxidative stress and TNF-α/TNFR1 signaling.