Heat shock response is associated with protection against acute interstitial pancreatitis in rats

Citation
H. Weber et al., Heat shock response is associated with protection against acute interstitial pancreatitis in rats, DIG DIS SCI, 45(11), 2000, pp. 2252-2264
Citations number
44
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
DIGESTIVE DISEASES AND SCIENCES
ISSN journal
01632116 → ACNP
Volume
45
Issue
11
Year of publication
2000
Pages
2252 - 2264
Database
ISI
SICI code
0163-2116(200011)45:11<2252:HSRIAW>2.0.ZU;2-M
Abstract
We recently reported that hyperthermia induces pancreatic expression of hea t shock proteins (HSPs), particularly HSP70 isoforms, and protects against cerulein pancreatitis. We have now studied whether a double hyperthermia am plifies these effects and whether hyperthermia also protects against dibuty ltin dichloride (DBTC)-induced pancreatitis. A further aim was to examine w hether hyperthermia induces changes in transforming growth factor-beta (1) (TGF-beta (1)), Following pretreatment without or with a single or double h yperthermia, pancreatitis was induced by application of cerulein or DBTC. P ancreatic HSP and TGF-beta (1) expression were studied by immunoblotting. P ancreas injury was assessed by light microscopy and serum pancreatic enzyme activity. Hyperthermia as well as DBTC induced HP72, whereas cerulein did not. A double hyperthermia led to a further increase in HSP72 compared to a single heat stress. In both models, hyperthermia significantly reduced pan creatic injury. Although a double hyperthermia slightly decreased the sever ity of cerulein pancreatitis compared to a single heat treatment, an improv ed pancreas protection against DBTC cytotoxicity was not achieved. We also found that hyperthermia induces the expression of TGF-beta (1) In conclusio n, hyperthermia preconditioning exerts protective effects against two patho physiologically different types of pancreatitis by a mechanism that involve s the up-regulation of IISP70 isoforms as well as TGF-beta (1).