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Figure Lengend Snippet: Validation of the anti-inflammatory efficacy of candidate drugs in LPS-primed and CSE-stimulated macrophages: ( A ) Schematic diagram of the 96-well plate layout showing the distribution of control, macrophage inflammatory model (MIM; LPS + CSE), and drug treatment groups across three independent replicates. ( B ) Heatmap representation of the raw concentration distribution across the 96-well plate, confirming consistent experimental conditions across all the wells. ( C ) Dose-dependent inhibition of IL-8 secretion by Celecoxib. Compared to the MIM group, Celecoxib treatment significantly reduced IL-8 levels in a concentration-dependent manner ( p = 0.0015 for low dose, p < 0.001 for medium and high doses). ( D ) Dose-dependent inhibition of IL-8 secretion by Lovastatin. Lovastatin administration significantly attenuated IL-8 release across all the tested concentrations ( p < 0.01 for all the doses). ( E ) Dose-dependent inhibition of IL-1β secretion by Celecoxib. Celecoxib robustly suppressed IL-1β levels, with medium and high doses achieving p < 0.001 compared to the MIM group. ( F ) Dose-dependent inhibition of IL-1β secretion by Lovastatin. Lovastatin significantly reduced IL-1β hypersecretion in a dose-dependent manner ( p < 0.01 for low dose, p < 0.001 for medium and high doses). Significance: * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Interleukin-8 (IL-8) was measured using the EasyGo Human IL-8 One-Step ELISA Kit (Cat. No. EK108EG, Multi Sciences, Hangzhou, China), and Interleukin-1β (IL-1β) was evaluated utilizing the Human IL-1β ELISA Kit (Cat. No. EK101B, Multi Sciences).

Techniques: Biomarker Discovery, Control, Concentration Assay, Inhibition

Journal: International journal of molecular medicine

Article Title: miR‑217 and miR‑543 downregulation mitigates inflammatory response and myocardial injury in children with viral myocarditis by regulating the SIRT1/AMPK/NF‑κB signaling pathway.

doi: 10.3892/ijmm.2019.4442

Figure Lengend Snippet: Figure 5. Role of miR‑217 and miR‑543 on CVB3‑infected H9C2 cells. H9C2 cells were transfected with miR‑217 or miR‑543 inhibitors, miR‑217 or miR‑543 inhibitor controls, miR‑217 inhibitor + SIRT1‑siRNA, or miR‑543 inhibitor + SIRT1‑siRNA for 48 h and then treated with 104 PFU/ml CVB3 virus for 48 h. Effects of (A) miR‑217 and (B) miR‑543 on cell viability of CVB3‑infected H9C2 cells. Effect of (C) miR‑217 and (D) miR‑543 on cell apoptosis of CVB3‑infected H9C2 cells. Effects of (E) miR‑217 and (F) miR‑543 on Bax and Bcl‑2 protein expression levels in CVB3‑infected H9C2 cells. *P<0.05, **P<0.01 vs. corresponding control; &P<0.05, &&P<0.01 vs. corresponding miR inhibitor. #P<0.05, ##P<0.01 vs. CVB3. CVB3, Coxsackievirus B3; miR, microRNA; SIRT1, sirtuin 1; siRNA, small interfering RNA; inhibitor control‑1, miR‑217 inhibitor control; inhibitor con- trol‑2, miR‑543 inhibitor control.

Article Snippet: The Annexin V-FITc/propidium iodide (PI) apoptosis detection kit (cat. no. 70-AP101-100; MultiSciences) was used to analyze cell apoptosis.

Techniques: Transfection, Virus, Expressing, Control, Small Interfering RNA