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1.
J Tradit Chin Med ; 42(1): 49-57, 2022 02.
Artículo en Inglés | MEDLINE | ID: mdl-35322632

RESUMEN

OBJECTIVE: To evaluate the therapeutic effectiveness of salidroside (Sal) and pyrrolidine dithiocarbamate (PDTC) against severe acute pancreatitis (SAP) in a rat model. METHODS: Rat models of SAP were established by retrograde infusion of sodium taurocholate solution. SAP rats were randomly divided into 6 groups: SAP 3 h group, SAP 24 h group, low-dose Sal treatment group (Sal L+S), middle-dose Sal treatment group (Sal M+S), high-dose Sal treatment group (Sal H+S) and PDTC treatment group (PDTC+S). The serum amylase, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and interleukin-10 (IL-10) levels were determined by optical turbidimetry and enzyme-linked immunosorbent assay. The expression of Beclin-1, microtubule-associated protein light chain 3II (LC3 II ), lysosome associated membrane protein 2 (LAMP2), interleukin-1 receptor associated kinase 1 (IRAK1) inhibitor α of nuclear transcription factor-kB (IkBα), nuclear transcription factor-kB 65 (p65) in the pancreas tissues were detected by quantitative real-time polymerase chain reaction and Western blot, while the pIkBα and p-p65 levels were detected by Western blot. Pathological changes of the pancreas and all the other indexes were observed at 3 and 24 h after operation. RESULTS: The serum IL-10 level, IkBα and LAMP2 levels in Sal M+S, Sal H+S and PDTC+S groups were higher than those in SAP 24 h group, while all the other indexes in these three groups were all lower significantly than those in SAP 24 h group. There was no significant difference in all indexes between Sal H+S and PDTC+S groups. CONCLUSION: High-dose Sal has an effectively therapeutic effect on SAP in rats, which was similar to PDTC.


Asunto(s)
Pancreatitis , Enfermedad Aguda , Animales , Glucósidos , Humanos , Interleucina-10/genética , FN-kappa B/genética , FN-kappa B/metabolismo , Pancreatitis/tratamiento farmacológico , Pancreatitis/patología , Fenoles , Pirrolidinas , Ratas , Ratas Sprague-Dawley , Tiocarbamatos , Factores de Transcripción/uso terapéutico , Factor de Necrosis Tumoral alfa/metabolismo
2.
World J Gastroenterol ; 14(10): 1504-9, 2008 Mar 14.
Artículo en Inglés | MEDLINE | ID: mdl-18330938

RESUMEN

AIM: To investigate apoptosis in human pancreatic cancer cells induced by Triptolide (TL), and the relationship between this apoptosis and expression of caspase-3' bcl-2 and bax. METHODS: Human pancreatic cancer cell line SW1990 was cultured in DMEM media for this study. MTT assay was used to determine the cell growth inhibitory rate in vitro. Flow cytometry and TUNEL assay were used to detect the apoptosis of human pancreatic cancer cells before and after TL treatment. RT-PCR was used to detect the expression of apoptosis-associated gene caspase-3' bcl-2 and bax. RESULTS: TL inhibited the growth of human pancreatic cancer cells in a dose-and time-dependent manner. TL induced human pancreatic cancer cells to undergo apoptosis with typically apoptotic characteristics. TUNEL assay showed that after the treatment of human pancreatic cancer cells with 40 ng/mL TL for 12 h and 24 h, the apoptotic rates of human pancreatic cancer cells increased significantly. RT-PCR demonstrated that caspase-3 and bax were significantly up-regulated in SW1990 cells treated with TL while bcl-2 mRNA was not. CONCLUSION: TL is able to induce the apoptosis in human pancreatic cancer cells. This apoptosis may be mediated by up-regulating the expression of apoptosis-associated caspase-3 and bax gene.


Asunto(s)
Adenocarcinoma/patología , Antineoplásicos Alquilantes/farmacología , Apoptosis/efectos de los fármacos , Diterpenos/farmacología , Medicamentos Herbarios Chinos/farmacología , Neoplasias Pancreáticas/patología , Fenantrenos/farmacología , Adenocarcinoma/metabolismo , Caspasa 3/metabolismo , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Compuestos Epoxi/farmacología , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Humanos , Neoplasias Pancreáticas/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , ARN Mensajero/metabolismo , Factores de Tiempo , Tripterygium , Regulación hacia Arriba/efectos de los fármacos , Proteína X Asociada a bcl-2/metabolismo
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