Amlodipine inhibits TNF-α production and attenuates cardiac dysfunction induced by lipopolysaccharide involving PI3K/Akt pathway

17β-estradiol attenuates homocysteine-induced oxidative stress and inflammatory response as well as MAPKs cascade via activating PI3-K/Akt signal transduction pathway in Raw 264.7 cells

“…The results demonstrate that the down-regulation of 17β-E 2 on inflammatory cytokines is in part dependent on PI3-K/Akt activation, and TNF-α and IL-1β are the downstream targets of PI3-K/Akt signal pathway. Additionally, inhibition of PI3-K can induce the expression of proinflammatory mediators and cytokines production in LPS or Hcy-stimulated microphages and cardiomyocytes and glomerular mesangial cells [16,43,44]. These reports further strengthen our findings, and demonstrate a pivotal role of PI3-K/Akt signaling in the regulation of proinflammatory cytokines in various cell types.…”

The comparison of α-bromo-4-chlorocinnamaldehyde and cinnamaldehyde on coxsackie virus B3-induced myocarditis and their mechanisms

“…Sections (4 μm thick) were placed on glass slides, and paraffin was removed by xylene [30]. Then, the tissue sections were stained with haematoxylin and eosin (H&E) reagent and were examined and photographed using a light microscope (Eclipse 80i, Nikon, Japan).…”

“…Whole-cell lysates were prepared according to the procedure previously described [30]. Samples containing equal amounts of protein were separated by 10% SDS-PAGE and transferred onto nitrocellulose membranes.…”

Madecassoside suppresses LPS-induced TNF-α production in cardiomyocytes through inhibition of ERK, p38, and NF-κB activity

“…After treated with varying concentrations of MA (0-300 µmol/l) for 2 h and then stimulated with 100 ng/ml of LPS for 12 h [12], cells (1 × 10 6 cells/well) were collected immediately and total RNA was extracted using Trizol reagent. One microgram of total RNA was reverse-transcribed into cDNA with 0.2 U/ml Superscript III reverse transcriptase according to the manufacturer's protocol.…”