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1 October 2000 The myocardial heat shock response following sodium salicylate treatment
Marius Locke, Joel Atance
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Abstract

In cultured cells, salicylate has been shown to potentiate the induction of Hsp72 so that a mild heat stress (40°C) in the presence of salicylate induces an Hsp72 response that is similar to a severe heat stress (42°C). To determine whether salicylate can potentiate the myocardial Hsp70 response in vivo and confer protection from an ischemic stress, male Sprague-Dawley rats (250–300 g) were placed into 5 groups: (1) control, (2) salicylate only (400 mg/kg), (3) mild heat stress (40°C for 15 minutes), (4) mild heat stress plus salicylate, and (5) severe heat stress (42°C for 15 minutes). Twenty-four hours following salicylate treatment and/or heat stress, animals were anesthetized, their hearts rapidly isolated, and hemodynamic function evaluated using the Langendorff technique. Hsp72 content was subsequently assessed by Western blotting. Although salicylate in combination with a mild heat stress induced heat shock factor activation, only the hearts from severely heat-stressed animals (42°C) demonstrated a significantly elevated myocardial Hsp72 content and a significantly enhanced postischemic recovery of left ventricular developed pressure and rates of contraction and relaxation. These results support the role for Hsp72 as a protective protein and suggest that neither salicylate treatment alone nor salicylate in combination with a mild heat stress potentiates the myocardial Hsp72 response.

Marius Locke and Joel Atance "The myocardial heat shock response following sodium salicylate treatment," Cell Stress & Chaperones 5(4), 359-368, (1 October 2000). https://doi.org/10.1379/1466-1268(2000)005<0359:TMHSRF>2.0.CO;2
Received: 1 May 2000; Accepted: 1 June 2000; Published: 1 October 2000
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