ABSTRACT
Recurrent pancreatitis ( RP) can be further divided into two items , including recurrent acute pancreatitis ( RAP ) and recurrent chronic pancreatitis ( RCP ) .In recent years, with the rising incidence of pancreatitis , the incidence of RP has also been increased .During the development of pancre-atic diseases, RP may serve as a transitional disease .Thus, this article reviewed the latest research progress on RP in order to discuss its role in the development of the related pancreatic di-seases and the effects on clinical prognosis , and provide a refe-rence for preventing and treating RP and even cancer .
ABSTRACT
Pancreatic acinar cell death modality is a significant factor which determines the course and prognosis of acute pancreatitis (AP).The severity of AP is positively correlated with acinar necrosis,while negatively correlated with acinar apoptosis.Adenosine triphosphate (ATP) level is the key to control the manner of death,and acts as a switch during the conversion of necrosis and apoptosis in a variety of pathophysiological settings:low levels of ATP can accelerate cell necrosis and high levels of ATP might promote apoptosis.Hypoxia inducible factor 1 (HIF-1) is a highly expressed transcription factor in anoxic conditions which can effectively regulate cell energy metabolism and play an important role in regulating cell death and inflammatory injury.Therefore,this review aimed to provide a reference about better understanding of the pathogenesis and new therapeutic targets of HIF-1 in AP.
ABSTRACT
Aim To investigate the anticancer activity and the mechanism of the apoptosis induced by Ama-ranthus spinosus L. extract ( ASE ) in human hepatic carcinoma cell line HepG2 . Methods Alamar blue assay was used for detecting the influence of ASE on the proliferation of the cancer cells. The morphological changes of cells were observed under inverted micro-scope and Hoechst 33258 stainning. The apoptosis of HepG2 cells was detected by flow cytometry. Western blot and caspase-3 activity kit were used to detect the protein expression in HepG2 cells. The specific inhibi-tor of caspase-9 and caspase-3 ( Z-LEHD-FMK and Ac-DEVD-CHO) was used to validate the signal transduc-tion pathyway. Results The results indicated that the cell proliferation was inhibited by ASE,especicially the HepG2 cells. The HepG2 cells showed obvious apop-totic characteristics. Flow cytometry analysis further validated the apoptosis of HepG2 cells. The expression of Bcl-2 and survivin was downreagulated in HepG2 cells treated with ASE, and Bax, caspase-9, caspase-3, Apaf-1 and PARP were upregualted. Besides, the caspase-3 activity was also increased. Z-LEHD-FMK and Ac-DEVD-CHO significantly increased the cell vi-abilty of HepG2 cells induced by ASE. Conclusion These results confirm that ASE induces the apoptosis of HepG2 through mitochondria-mediated pathway.