RESUMO
There is no specific drug to treat severe acute pancreatitis (SAP), which induces substantial medical and social burden. Many studies have reported the beneficial effects of emodin against SAP in vivo and in vitro. However, the underlying mechanism has been unclear. This paper described the design and implementation of anti-inflammatory and antioxidant activity of emodin. Emodin restored the pathological damage of SAP and simultaneously decreased the high levels of serum amylase, lipase, TNF-α, and IL-18 in the peripheral blood of SAP rat. Emodin reversed reactive oxygen species (ROS) in neutrophils derived from SAP rat. The levels of voltage-dependent anion channel 1 (VDAC1), NOD-like receptor protein 3 (NLRP3), caspase-1, and IL-18 were examined to analyze the change of inflammasome-related mediators between SAP and emodin treatment. These findings suggest that emodin plays its protective role on SAP against oxidative stress and inflammasome signals.
Assuntos
Anti-Inflamatórios/farmacologia , Antioxidantes/farmacologia , Emodina/farmacologia , Pancreatite/tratamento farmacológico , Amilases/sangue , Animais , Anti-Inflamatórios/uso terapêutico , Antioxidantes/uso terapêutico , Emodina/uso terapêutico , Humanos , Inflamassomos/efeitos dos fármacos , Inflamassomos/metabolismo , Interleucina-18/sangue , Estresse Oxidativo/efeitos dos fármacos , Inibidores de Proteínas Quinases/farmacologia , Ratos , Fator de Necrose Tumoral alfa/sangueRESUMO
Pancreatic diseases, such as acute pancreatitis, chronic pancreatitis, and pancreatic cancer, are common gastrointestinal diseases resulting in the development of local and systemic complications with a high risk of death. Numerous studies have examined pancreatic diseases over the past few decades; however, the pathogenesis remains unclear, and there is a lack of effective treatment options. Recently, emerging evidence has suggested that transforming growth factor beta (TGF-ß) exerts controversial functions in apoptosis, inflammatory responses, and carcinogenesis, indicating its complex role in the pathogenesis of pancreas-associated disease. Therefore, a further understanding of relevant TGF-ß signalling will provide new ideas and potential therapeutic targets for preventing disease progression. This is the first systematic review of recent data from animal and human clinical studies focusing on TGF-ß signalling in pancreas damage and diseases. This information may aid in the development of therapeutic agents for regulating TGF-ß in this pathology to prevent or treat pancreatic diseases.