phillygenin and Inflammation

Ulcerative colitis (UC) is a chronic, relapsing, and nonspecific inflammatory bowel disease (IBD). Phillygenin (PHI), a natural bioactive ingredient, isolated from

Topics: Animals; Antiporters; Colitis; Colitis, Ulcerative; Colon; Dextran Sulfate; Genes, src; Inflammation; Mice; Mice, Inbred C57BL; Mitogen-Activated Protein Kinases; NF-kappa B; Signal Transduction; Sulfate Transporters; Toll-Like Receptor 4

Lipophagy is an autophagic process, which delivers the intracellular lipid droplets to the lysosomes for degradation. Recent studies revealed that the impairment of lysosomal biogenesis and autophagic flux led to dysregulation of lipophagy in hepatocytes, which exacerbated the development of nonalcoholic fatty liver disease (NAFLD). Therefore, agents restoring autophagic flux and lipophagy in hepatocytes may have therapeutic potential against this increasingly prevalent disease. Phillygenin (PHI), a lignin extracted from Forsythia suspense, exerts hepatoprotective and anti-inflammatory effects. However, the effect of PHI on NAFLD remains unknown.. This study aimed to investigate the protective effect of PHI on NAFLD and elucidate the underlying mechanism.. The effects of PHI were examined in palmitate (PA)-stimulated AML12 cells and primary hepatocytes, as well as in NAFLD mice induced by a high-fat diet (HFD). We also used transcription factor EB (TFEB) knockdown hepatocytes and hepatocyte-specific TFEB knockout (TFEB. Our results indicated that autophagic flux and lysosome biogenesis in PA-stimulated hepatocytes were impaired. PHI alleviated lipid deposition by increasing lysosomal biogenesis and autophagic flux. It also stimulated the release of endoplasmic reticulum Ca. Despite PHI has been reported to have anti-hepatic fibrosis effects, whether it has a hepatoprotective effects against NAFLD and the underlying molecular mechanism remain unclear. Herein, we found that PHI restored lipophagy and suppressed lipid accumulation and inflammation by regulating the Ca

Topics: Animals; Autophagy; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; Calcineurin; Hepatocytes; Inflammation; Lignans; Lipids; Lysosomes; Mice; Non-alcoholic Fatty Liver Disease

Forsythia suspensa (Thunb.) Vahl (Oleaceae) leaves are valuable sources of phillygenin. This study aimed to isolate phillygenin from F. suspensa leaves and examine its analgesic and anti-inflammatory effects. Phillygenin was successfully extracted and isolated from F. suspensa leaves after fermentation. Phillygenin significantly reduced the number of writhing induced by acetic acid, prolonged the latency period in the hot plate test, and inhibited the xylene-induced ear edema and carrageenan-induced paw edema in mice. IL-6, TNF-α, IL-1β, NO, and PGE

Topics: Analgesics; Animals; Anti-Inflammatory Agents; Carrageenan; Edema; Forsythia; Inflammation; Mice; Pain; Plant Extracts

Acute lung injury (ALI) is often responsible for the high morbidity of critically ill patients. The present study aimed to investigate whether phillygenin (PHI) can inhibit inflammation and apoptosis of pulmonary epithelial cells by activating peroxisome proliferator‑activated receptor γ (PPARγ) signaling. The

Topics: Acute Lung Injury; Anti-Inflammatory Agents; Apoptosis; Cell Line; Child; Child, Preschool; Epithelial Cells; Female; Humans; Inflammation; Lignans; Male; Matrix Metalloproteinase 8; PPAR gamma

Inflammation is a common pathological phenomenon when homeostasis is seriously disturbed. Phillygenin (PHI), a lignin component isolated from Forsythiae Fructus, has shown a good anti-inflammatory effect. However, the mechanisms of PHI on anti-inflammation have not yet been systematically elucidated. In this study, the lipopolysaccharide (LPS) - induced RAW264.7 cell inflammation model was established to investigate mechanisms of PHI on inflammation. The effect of PHI on the release of IL-1β and PGE2 inflammatory factors induced by LPS was detected by ELISA, and the mRNA expressions of IL-1β, IL-6 and TNF-α were detected by RT-qPCR. Proteomics studied the signaling pathways that might be affected by PHI and molecular docking technology was subsequently used to study the possible targets on proteomic screened pathways. Western blot was performed ultimately to detect progressive changes in protein expression on the related pathway. Our research showed that PHI significantly inhibited the robust increase of IL-1β and PGE2 and lowered the transcriptional level of inflammatory genes including IL-6, IL-1β and PGE2 in LPS-stimulated RAW264.7 cells. Proteomics results indicated that PHI was involved in the regulation of multiple signaling pathways. Molecular docking results indicated that PHI had an affinity for most proteins in NF-κB pathway. Western blot analysis proved that PHI inhibited LPS-induced NF-κB pathway activation. On the whole, PHI inhibited the activation of NF-κB pathway, thereby inhibiting the expression of related inflammatory genes and the release of cytokines, and showed a remarkable anti-inflammatory effect.

Topics: Animals; Anti-Inflammatory Agents; Cytokines; Dinoprostone; Inflammation; Inflammation Mediators; Lignans; Lipopolysaccharides; Macrophages; Mice; Molecular Docking Simulation; NF-kappa B; Protein Interaction Maps; Proteomics; RAW 264.7 Cells; Signal Transduction