Pancreatitis is an inflammatory disease of the exocrine pancreas with considerable morbidity and mortality and without specific treatment. Current studies show the involvement of lysosomes in the pathophysiology of pancreatitis. Lysosomal dysfunction in pancreatitis is manifested by decreased maturation of histone B and histone L, increased autophagosome formation and decreased lysosomal degradation. Lysosomal/autophagic dysfunction is a key initiating event in pancreatitis and a confluence of multiple disordered pathways. The study of autophagy in pancreatitis is just in its infancy, and many questions about the pathological link between mediated lysosomal/autophagic dysfunction and pancreatitis remain to be explored. Addressing these questions will help provide insight into new molecular targets and therapeutic strategies for the treatment of pancreatitis.
Fig. 1. Lysosomal dysfunction leads to autophagy impairment and other pathologic responses of pancreatitis. (Gukovsky I, et al., 2012)
Lysosomal Function Analysis Services in Pancreatitis
CD BioSciences is committed to providing our global clients with a comprehensive service to analyze lysosomal changes and dysfunction in pancreatitis through the detection of lysosomal enzyme activity and lysosomal membrane proteins, and the identification of autophagy-related genes. Our aim is to evaluate changes in several lysosomal enzyme activities and lysosomal membrane proteins in the rat kidney during experimental acute pancreatitis, including histone B, histone L, LAMP-1 and LAMP-2.
Our scientists establish proven alternative in vivo and in vitro models of pancreatitis.
- Rodent model of non-alcoholic acute pancreatitis
Pancreatitis induced in rats or mice by administration of high doses of rainfarin (an analogue of CCK-8), L-arginine, or bile acids. In young mice by feeding a choline-deficient, ethionine-supplemented diet. - Alcoholic pancreatitis model
Mixing ethanol feeding with low doses of caerulein or LPS caused significant pancreatic injury in rodents. - Pancreatitis in vitro model
Lysosomal subpopulations were isolated from mouse or rat pancreas by stimulation with rainfrogin or bile acids, and the stability of lysosomal membranes was assessed.
In addition, we collaborated with international cytologists to use genetic, molecular (small interfering RNA) and pharmacological approaches to develop mouse strains lacking key autophagy proteins such as Atg5, Beclin1 and Atg7. We assessed lysosomal autophagic changes in pancreatitis by assaying autophagic fluxes, applicable to tissue measurements and simultaneously determining changes in LC3 protein.
Our Available Technologies
- Transmission Electron Microscopy
- Gene Knockdown Techniques
- Small Interfering RNA (siRNA)
- Pharmacological Methods
Advantages of Our Services
- Multiple cutting-edge technologies.
- Fast and simple experimental procedures, delivered at an economical price.
- Team with expertise, working with international experts.
- Proven in vivo and in vitro models of experimental pancreatitis.
- Exploration of potential lysosome-related molecular targets for treating or reducing the severity of pancreatitis.
Our professional services for the analysis of lysosomal changes and dysfunction in pancreatitis have been well received by customers. Our highly skilled and dedicated scientific staff ensures that the most appropriate method and technology is selected for each specialized lysosomal project. If you have any special requirements about our services, please feel free to contact us. We are looking forward to working together with your attractive projects.
Reference
- Gukovsky I, et al. (2012) Impaired autophagy and organellar dysfunction in pancreatitis. J Gastroenterol Hepatol. 27 Suppl 2(Suppl 2):27-32.