Puerarin Ameliorates Ferroptosis in Neuronal Injury Through the PI3K/AKT Signaling Pathway.

Ferroptosis plays an important role in the pathogenesis of neuronal damage, generally mediated by iron and lipid peroxidation. In the present study, we measured the protective effects of puerarin against corticosterone-induced neuronal injury PI3K/AKT-mediated activation of nuclear factor erythroid 2-related factor 2 (Nrf2). After exposing corticosterone-treated PC12 cells to indicated compounds, we measured the key regulators of ferroptosis (ferritin, SLC7A11, and Ptgs2), ferroptosis events (levels of iron, ROS, MDA, and GSH), and the PI3K/AKT/Nrf2 axis.

Sulforaphane suppresses cell proliferation and induces apoptosis in glioma via the ACTL6A/PGK1 axis.

This study aimed to examine the expression and biological functions of ACTL6A in glioma cells (U251), the effects of sulforaphane on the growth of U251 cells and the involvement of the ACTL6A/PGK1 pathway in those effects. The U251 cell line was transfected with ACTL6A over-expression plasmids to upregulate the protein, or with ACTL6A inhibitor to underexpress it, then treated with different concentrations of sulforaphane. Cell viability, proliferation, and apoptosis were assessed using standard assays, and levels of mRNAs encoding ACTL6A, PGK1, cyclin D1, Myc, Bax or Bcl-2 were measured using quantitative real-time polymerase chain reaction (qRT-PCR).

Puerarin attenuates LPS-induced inflammatory injury in gastric epithelial cells by repressing NLRP3 inflammasome-mediated apoptosis.

The NLRP3 inflammasome plays a crucial role in microbially induced gastric epithelial injury, but the underlying mechanisms remain unclear. Here, we aimed to assess the impacts of puerarin on LPS-induced inflammatory damage and the involvement of the AMPK/SIRT1/NLRP3 signaling pathways in this process in GES-1 cells. Cell viability and cytotoxicity were determined using CCK-8 and lactate dehydrogenase assay kits.

Sulforaphane suppresses autophagy during the malignant progression of gastric carcinoma via activating miR-4521/PIK3R3 pathway.

Objective: Sulforaphane, which exerts an effective anti-cancer ability, is a phytochemical converted from cruciferous plants. Here, we aimed to identify whether sulforaphane could suppress autophagy during the malignant progression of gastric carcinoma and to explore the underlying mechanisms.

Methods: SGC7901 cells were transfected with miR-4521 mimics, inhibitor, and pcDNA3.

STAT3/miR-15a-5p/CX3CL1 Loop Regulates Proliferation and Migration of Vascular Endothelial Cells in Atherosclerosis.

Endothelial cell proliferation disorder caused by vascular injury seems to be one of the causes of atherosclerosis, which is the pathological basis of coronary heart disease. The role of STAT3 in the regulation of microRNAs and endothelial dysfunction in atherosclerosis is unclear. STAT3 can be activated by cytokine IL-6 and up regulate the expression of CX3CL1.