galloylpaeoniflorin and Inflammation

To assess the therapeutic effect and mechanism of 6'-o-galloylpaeoniflorin (GPF) in pediatric pneumonia.. The effects of lipopolysaccharide (LPS) and GPF on cell viability and apoptosis were examined by cell counting kit-8 assay and flow cytometry analysis. The oxidative stress and inflammatory response were assessed by detecting expression levels of superoxide dismutase, glutathione, r-glutamyl cysteingl+glycine, myeloperoxidase, and malondialdehyde as well as tumor necrosis factor-α, Interleukin-18, and Interleukin-10 by using enzyme-linked-immunosorbent serologic assay. Moreover, the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway was detected by immunoblot assay, and the influence of Nrf2-knockdown on cell viability, oxidative stress, and inflammation response was also investigated.. The results established that GPF increased the viability of LPS-induced pneumonia cells. In addition, GPF reduced LPS-induced oxidative stress in pneumonia cells. It was further discovered that GPF reduced LPS-induced inflammation in pneumonic cell. GPF improved the activity of Nrf2 in LPS-treated pneumonic cells, and therefore alleviated inflammation and oxidative stress in pediatric pneumonia.. GPF could serve as a promising drug for treating pediatric pneumonia.

Topics: Bridged Bicyclo Compounds, Heterocyclic; Child; Glucosides; Humans; Inflammation; Lipopolysaccharides; Monoterpenes; NF-E2-Related Factor 2; Oxidative Stress; Pneumonia; Signal Transduction

As a common disease of the digestive system, chronic gastritis is inflammation of the gastric mucosa caused by various factors. Helicobacter pylori (H. pylori) is one of the main causes of chronic gastritis, which can lead to gastric mucosal damage and gland atrophy, thereby promoting gastrocarcinogenesis. Oxidative stress and the inflammatory response are important mechanisms of H. pylori-induced gastritis. 6'-O-Galloylpaeoniflorin (GPF) is a substance isolated from peony root with antioxidant and anti-inflammatory activities. However, its role and mechanism in the pathogenesis of H. pylori-induced chronic gastritis remain unclear. This study explored the effects of GPF on H. pylori-induced gastric mucosal oxidative stress and inflammation using flow cytometry, western blotting, real-time quantitative PCR, and immunohistochemistry. We found that H. pylori infection increased oxidative stress and expression of inflammatory cytokines in vitro and in vivo and that these outcomes were inhibited by GPF. Furthermore, GPF activated nuclear factor erythroid-related factor-2 (Nrf2) and its downstream target genes in H. pylori-infected GES-1 cells and mice. The anti-inflammatory and antioxidant effects of GPF on H. pylori-infected cells were attenuated by an Nrf2 inhibitor. Taken together, these data suggest that GPF reduces H. pylori-induced gastric mucosa injury by activating Nrf2 signaling and that GPF is a potential candidate for the treatment of H. pylori-associated gastritis.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Bridged Bicyclo Compounds, Heterocyclic; Gastric Mucosa; Gastritis; Glucosides; Helicobacter Infections; Helicobacter pylori; Inflammation; Mice; Monoterpenes; NF-E2-Related Factor 2