Catalpol Ameliorates Sodium Taurocholate-Induced Acute Pancreatitis in Rats via Inhibiting Activation of Nuclear Factor Kappa B

Autor: Yan Ling Hu, Rong Wan, Xing Peng Wang, Lei Qiu, De Qing Wu, Guo Jian Yin, Ge Yu, Wen Qin Xiao, Miao Xing, Xiao Feng Cang, Yu Ting Fan, Guo Yong Hu
Jazyk: angličtina
Rok vydání: 2014
Předmět:
Male
Iridoid
inflammatory cytokines
Interleukin-1beta
catalpol
Acinar Cells
NF-κB
lcsh:Chemistry
Rats
Sprague-Dawley

chemistry.chemical_compound
NF-kB
lcsh:QH301-705.5
Spectroscopy
biology
Chemistry
Pancreatitis
Acute Necrotizing

NF-kappa B
Interleukin
General Medicine
Computer Science Applications
Myeloperoxidase
Amylases
Taurocholic Acid
medicine.medical_specialty
acute pancreatitis
medicine.drug_class
Iridoid Glucosides
Catalysis
Article
Inorganic Chemistry
Internal medicine
medicine
Animals
Physical and Theoretical Chemistry
Interleukin 6
Molecular Biology
Peroxidase
Interleukin-6
Tumor Necrosis Factor-alpha
Organic Chemistry
Lipase
Rehmannia glutinosa
biology.organism_classification
medicine.disease
Taurocholic acid
Catalpol
Rats
Endocrinology
lcsh:Biology (General)
lcsh:QD1-999
biology.protein
Pancreatitis
Zdroj: International Journal of Molecular Sciences
Volume 15
Issue 7
Pages 11957-11972
International Journal of Molecular Sciences, Vol 15, Iss 7, Pp 11957-11972 (2014)
ISSN: 1422-0067
Popis: Catalpol, an iridoid glucoside extracted from the traditional Chinese herbal medicine, Rehmannia glutinosa, is reported to exert neuroprotective, anti-inflammatory, anti-tumor and anti-apoptotic effects. The main aim of the present study was to investigate whether catalpol ameliorates experimental acute pancreatitis (AP) induced by sodium taurocholate (STC). AP was induced in rats via retrograde injection of 4% STC (0.1 mL/100 g) into the biliopancreatic duct. Rats were pre-treated with saline or catalpol (50 mg/kg) 2 h before STC injection. At 12, 24 and 48 h after injection, the severity of AP was evaluated using biochemical and morphological analyses. Pretreatment with catalpol led to a significant reduction in serum amylase and lipase activities, pancreatic histological damage, myeloperoxidase (MPO) activity, interleukin (IL)-1β, IL-6 and TNF-α levels, and activation of nuclear factor kappa B (NF-κB). Moreover, administration of catalpol increased the viability of pancreatic acinar cells and inhibited NF-κB expression in vitro. Our results collectively support the potential of catalpol as a highly effective therapeutic agent for treatment of AP.
Databáze: OpenAIRE