Dapagliflozin Protects H9c2 Cells Against Injury Induced by Lipopolysaccharide via Suppression of CX3CL1/CX3CR1 Axis and NF-κB Activity.

Background: Dapagliflozin, a selective Sodium-glucose cotransporter-2 (SGLT2) inhibitor, has been shown to play a key role in the control and management of metabolic and cardiac diseases.

Objective: The current study aims to address the effects of dapagliflozin on the expression of fractalkine (FKN), known as CX3CL1, and its receptors CX3CR1, Nuclear factor-kappa B(NF-κB) p65 activity, Reactive oxygen species (ROS), and inflammation in LPS-treated H9c2 cell line.

Methods: H9c2 cells were cultured with lipopolysaccharide (LPS) to establish a model of LPS-induced damage, and then, subsequently were treated with dapagliflozin for 72 h.

Amnion membrane proteins attenuate LPS-induced inflammation and apoptosis by inhibiting TLR4/NF-κB pathway and repressing MicroRNA-155 in rat H9c2 cells.

Objective: Amnion membrane (AM) has been popular for the treatment of inflammatory disorders due to its cell repairing properties. This current study aims to find the underlying mechanisms of amnion membrane proteins (AMPs) against the pro-inflammatory miRNA, miR-155, miR-146, and anti-apoptotic microRNA, miR-21, in LPS-treated H9c2 cells.

Methods: Cell viability and apoptosis were determined by MTT assay and annexin V/PI staining.

Sulforaphane modulates CX3CL1/CX3CR1 axis and inflammation in palmitic acid-induced cell injury in C2C12 skeletal muscle cells.

Studies have shown that sulforaphane (SFN) has potent anti-inflammatory and free radical scavenging effects on obesity and associated disorder such as diabetes, polycystic ovary syndrome, and metabolic syndrome. fractalkine (CX3CL1) and its receptor, CX3CR1, play an important role in muscle metabolism by improving insulin-sensitizing effects. Here, in this study we examined the SFN effect on CX3CL1 and its receptor, CX3CR1, in C2C12 myotubes in palmitic acid (PA)-induced oxidative stress and inflammation.

ANN QSAR workflow for predicting the inhibition of HIV-1 reverse transcriptase by pyridinone non-nucleoside derivatives.

Aim: Pyridinone derivatives have high potency against non-nucleoside reverse transcriptase inhibitor (NNRTI)-resistant human immunodeficiency virus type-1 strains. Quantitative structure-activity relationship (QSAR) studies on a series of pyridinone derivatives acting as NNRTIs are very important in designing the next generation of NNRTIs. Methodology & results: The QSAR models were developed using linear (single and forward stepwise) and combined nonlinear artificial neural network (ANN) approaches.