Specific induction of a 72-kDa heat shock protein protects esophageal mucosa from reflux esophagitis

• Published in: Life sciences (1973) Vol. 84; no. 15; pp. 517 - 522
• Main Authors: Izumi, Yuko, Otaka, Michiro, Takahashi, Taiji, Takada, Makiko, Shimada, Yuji, Asaoka, Daisuke, Nagahara, Akihito, Itoh, Hideaki, Watanabe, Sumio
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 10.04.2009
• Subjects: Animals; Blotting, Western; Disease Models, Animal; Esophagitis, Peptic - metabolism; Esophagitis, Peptic - prevention & control; Esophagus; Heat shock protein; HSP72 Heat-Shock Proteins - biosynthesis; Hyperthermia; Hyperthermia, Induced; Male; Mucous Membrane - metabolism; Rats; Rats, Sprague-Dawley; Reflux esophagitis; Hyperthermia; Reflux esophagitis; Heat shock protein; Esophagus
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2009.01.016

The aim of this study is to investigate the expression and cytoprotective function of a 72-kDa heat shock protein (HSP72) using a reflux esophagitis model in rats. Expression of HSP60, HSP72, and HSP90 in rat esophageal mucosa was evaluated by Western blot analysis before and after hyperthermia (42.5 °C, 20 min). Rats received the operation to produce reflux esophagitis with or without pretreatment with hyperthermia to induce HSPs. The esophageal mucosal damage was evaluated 12 h after the operation. Expression of HSP72 was significantly increased by hyperthermia in rat esophageal mucosa. Reflux esophagitis was dramatically prevented when HSP72 was preinduced by hyperthermia. Furthermore, activation of TNF-α and IL-1β in esophageal mucosa was also suppressed. These results suggested that hyperthermia protects the esophageal mucosa in reflux esophagitis model by inducing HSP72 and suppressing proinflammatory cytokine activation. These findings might suggest that HSP-inducing therapy could be a novel and unique therapy for reflux esophagitis.