Kokura S, Yoshida N, Okuda T, Nakabe N, Sakamoto N, Isozaki Y, Hattori T, Handa O, Takagi T, Naito Y, Yoshikawa T
Department of Biomedical Safety Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Int J Hyperthermia. 2007 Feb;23(1):17-28. doi: 10.1080/02656730601090223.
Hyperthermia is known to protect against cellular injury through the expression of heat shock proteins. In this study, the therapeutic effects of hyperthermia on experimental colitis in the rat were evaluated.
Male Wistar rats were given a single intracolonic injection of 2,4,6-trinitrobenzene sulphonic acid (TNBS). Hyperthermia was induced in anesthetized rats by placing them in a temperature-controlled water bath. We started the hyperthermic treatment on the day after the enema. The severity of colitis was evaluated pathologically, and the activities of tissue myeloperoxidase were measured 6 days after the induction of colitis. Furthermore, cytokines, and hyperthermia-induced heat shock proteins in colonic mucosa were detected by enzyme-linked immunosorbent assay and Western blotting. We also investigated the effects of geranylgeranylacetone and zinc protoporphyrin IX on the therapeutic effect of hyperthermia.
Hyperthermia significantly improved the macroscopic scores of colitis. The TNBS-induced increases in the activities of myeloperoxidase in the colonic tissue were blunted significantly in hyperthermia-treated animals. Furthermore, hyperthermia attenuated increases in cytokine-induced neutrophil chemoattractants-1 and tumor necrosis factor-alpha in the colon. Furthermore, hyperthermia induced the production of heat shock proteins in rat colonic mucosa, and the combination of geranylgeranylacetone with hyperthermia further induced the heat shock protein HSP70, which resulted in further improvement of TNBS-induced colitis. On the other hand, the combination of zinc protoporphyrin IX with hyperthermia attenuated the therapeutic effect of hyperthermia.
Hyperthermia ameliorates TNBS-induced colitis in rats through the expression of HSP70 and HO-1. It is postulated that hyperthermia may be useful for the treatment of inflammatory bowel diseases.
已知热疗可通过热休克蛋白的表达来保护细胞免受损伤。在本研究中，评估了热疗对大鼠实验性结肠炎的治疗效果。
给雄性Wistar大鼠结肠内单次注射2,4,6-三硝基苯磺酸（TNBS）。将麻醉的大鼠置于温度可控的水浴中诱导热疗。灌肠后第二天开始热疗。对结肠炎的严重程度进行病理评估，并在诱导结肠炎6天后测量组织髓过氧化物酶的活性。此外，通过酶联免疫吸附测定和蛋白质印迹法检测结肠黏膜中的细胞因子和热疗诱导的热休克蛋白。我们还研究了香叶基香叶基丙酮和锌原卟啉IX对热疗治疗效果的影响。
热疗显著改善了结肠炎的宏观评分。在热疗治疗的动物中，TNBS诱导的结肠组织中髓过氧化物酶活性的增加明显减弱。此外，热疗减轻了结肠中细胞因子诱导的中性粒细胞趋化因子-⒈和肿瘤坏死因子-α的增加。此外，热疗诱导大鼠结肠黏膜中热休克蛋白的产生，香叶基香叶基丙酮与热疗联合进一步诱导热休克蛋白HSP70，从而使TNBS诱导的结肠炎得到进一步改善。另一方面，锌原卟啉IX与热疗联合减弱了热疗的治疗效果。
热疗通过HSP70和HO-⒈的表达改善TNBS诱导的大鼠结肠炎。据推测，热疗可能对炎症性肠病的治疗有用。
Zotero 插件