Frossard J-L, Bhagat L, Lee H S, Hietaranta A J, Singh V P, Song A M, Steer M L, Saluja A K
Division of Gastroenterology, Geneva University Hospitals, 1211 Geneva 14, Switzerland.
Gut. 2002 Jan;50(1):78-83. doi: 10.1136/gut.50.1.78.
Recent studies have indicated that prior thermal stress causes upregulation of heat shock protein 70 (HSP70) expression in the pancreas and protects against secretagogue induced pancreatitis. The mechanisms responsible for the protective effect are not known. Similarly, the effects of prior non-thermal stress on HSP70 expression and pancreatitis are not known. The current studies were designed to specifically address these issues.
In the current studies pancreatitis was induced by administration of a supramaximally stimulating dose of caerulein 12 hours after thermal stress and 24 hours after non-thermal (that is, beta adrenergic stimulation) stress.
Both thermal and non-thermal stresses caused pancreatic HSP70 levels to rise and resulted in increased expression of HSP70 in acinar cells. Both forms of stresses protected against caerulein induced pancreatitis and prevented the early intrapancreatic activation of trypsinogen which occurs in this model of pancreatitis.
These results suggest that both thermal and non-thermal stresses protect against pancreatitis by preventing intrapancreatic digestive enzyme activation and that HSP70 may mediate this protective effect.
近期研究表明，预先的热应激可导致胰腺中热休克蛋白70（HSP70）表达上调，并预防促分泌素诱导的胰腺炎。其保护作用的机制尚不清楚。同样，预先的非热应激对HSP70表达及胰腺炎的影响也不清楚。当前研究旨在专门解决这些问题。
在当前研究中，分别在热应激后12小时以及非热（即β肾上腺素能刺激）应激后24小时，通过给予超最大刺激剂量的雨蛙肽诱导胰腺炎。
热应激和非热应激均导致胰腺HSP70水平升高，并使腺泡细胞中HSP70的表达增加。两种应激形式均能预防雨蛙肽诱导的胰腺炎，并阻止在该胰腺炎模型中发生的胰蛋白酶原早期胰腺内激活。
这些结果表明，热应激和非热应激均通过防止胰腺内消化酶激活来预防胰腺炎，且HSP70可能介导这种保护作用。
