demethylzeylasteral has been researched along with Inflammation* in 3 studies
3 other study(ies) available for demethylzeylasteral and Inflammation
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Demethylzeylasteral attenuates hepatic stellate cell activation and liver fibrosis by inhibiting AGAP2 mediated signaling.
Liver fibrosis is a common cause of chronic liver disease. If left untreated, it can ultimately develop into liver cirrhosis or hepatocellular carcinoma. However, a direct antifibrotic therapy is currently unavailable. A re-examination of existing chemicals might be a potential strategy for finding more lead compounds against liver fibrosis. Demethylzeylasteral (T-96), a naturally occurring bioactive compound found in Tripterygium wilfordii Hook. f. (TwHf) possesses multiple pharmacological properties. However, its antifibrotic potential has not yet been fully evaluated.. This study aimed to investigate the antifibrotic properties of T-96 and its underlying molecular mechanisms.. The T-96 treatment significantly suppressed the proliferation, migration, and activation of HSCs in vitro. The administration of T-96 attenuated hepatic injury, inflammation, and fibrosis progression in mice with CCl. Our results provide the first insight that T-96 exerts potent antifibrotic effects both in vitro and in vivo by inhibiting the AGAP2 mediated FAK/AKT signaling axis, and that T-96 may serve as a potential therapeutic candidate for the treatment of liver fibrosis. Topics: Animals; Fibrosis; Hepatic Stellate Cells; Inflammation; Liver; Liver Cirrhosis; Mice; Proto-Oncogene Proteins c-akt; Triterpenes | 2022 |
T-96 attenuates inflammation by inhibiting NF-κB in adjuvant-induced arthritis.
The extract of the medicinal plant, Topics: Animals; Apoptosis; Arthritis, Experimental; Arthritis, Rheumatoid; Cells, Cultured; Cytokines; Dose-Response Relationship, Drug; Fibroblasts; Inflammation; Molecular Structure; NF-kappa B; Plants, Medicinal; Rats, Sprague-Dawley; Synovial Membrane; Tripterygium; Triterpenes | 2020 |
Demethylzeylasteral ameliorates inflammation in a rat model of unilateral ureteral obstruction through inhibiting activation of the NF‑κB pathway.
The present study investigated the pharmacodynamic role and therapeutic mechanism of demethylzeylasteral in the suppression of inflammation in a rat model of unilateral ureteral obstruction and reduction in nuclear factor (NF)‑κB pathway activity. The rats in the unilateral ureteral obstruction model were treated with 30‑120 mg/kg demethylzeylasteral for 8 weeks. The activities of tumor necrosis factor (TNF)‑α, interleukin (IL)‑6 and caspase‑3/9, and the protein expression levels of cyclooxygenase (COX)‑2 and intercellular adhesion molecule‑1 (ICAM‑1) and NF‑κB p65 were analyzed using ELISA kits and western blot analyses, respectively. Compared with the rats in the unilateral ureteral obstruction model group, demethylzeylasteral treatment markedly inhibited the increased concentrations of serum creatinine and blood urea nitrogen, urinary protein/creatinine ratio, and concentrations of high‑density lipoprotein and low‑density lipoprotein cholesterol, and prevented kidney damage. In addition, demethylzeylasteral inhibited the levels of TNF‑α andIL‑6 and suppressed the protein expression levels of COX‑2 and ICAM‑1 in the kidneys of the rats in the unilateral ureteral obstruction model. Demethylzeylasteral also significantly suppressed the protein expression of NF‑κB p65. The results of the present study suggested that demethylzeylasteral unilateral ureteral obstruction and inhibited inflammation via inhibiting the activation of COX‑2, ICAM‑1 and NF‑κB p65, and suppressing the activities of caspase‑3/9 in rats with unilateral ureteral obstruction. Topics: Animals; Anti-Inflammatory Agents; Biomarkers; Caspase 3; Caspase 9; Cyclooxygenase 2; Cytokines; Disease Models, Animal; Inflammation; Inflammation Mediators; Intercellular Adhesion Molecule-1; Kidney; Male; NF-kappa B; Rats; Signal Transduction; Triterpenes; Ureteral Obstruction | 2017 |