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題 名 | Heat Shock Treatment Decreases the Mortality of Sepsis in Rats=熱休克前處置降低大白鼠敗血症的死亡率 |
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作 者 | 楊瑞成; 王純鶯; 陳香文; 周封百; 呂勝義; 黃高彬; | 書刊名 | The Kaohsiung Journal of Medical Sciences |
卷 期 | 14:11 1998.11[民87.11] |
頁 次 | 頁664-672 |
分類號 | 414.82 |
關鍵詞 | 大白鼠; 敗血症; 熱休克蛋白質; Heat shock protein 72; Sepsis; Rats; |
語 文 | 英文(English) |
中文摘要 | 近年來熱休克蛋白質已被廣泛探討並接受為當細胞處於窘迫時會自行誘發的一群蛋白質,藉著這種蛋白質的產生,可以保護細胞甚至個體免於繼發的惡劣環境。在本研究,吾等嘗試探討敗血症的大鼠模式中不同時期(早期及晚期),大鼠體內熱休克蛋白質誘發合成的情形;並探討術前熱休克蛋白質的存在下,對於敗血症大鼠的死亡率的影響。實驗動物使用成熟雄性S-D大鼠。體內及體外熱休克處置係分別以全身電毯加熱法及恆溫水浴法為之。 敗血症的誘發則採用大腸結紮及穿孔術。熱休克蛋白質的偵測則是取動物各主要器官及淋巴球,經蛋白質之萃取、電氣泳動分離、西方轉漬及免疫化學染免法呈色之。結果顯示:在早期及晚期敗血症中,大鼠體內均無熱休克蛋白質的增生;但是若將淋巴球施以一足量的窘迫,如於體外加熱至攝氏42度,則可誘發其合成。當術前利用全身加熱法誘發熱休克蛋白質大量表現的情況下,明顯的可以降低敗血症大鼠的死亡率。由以上結果,吾等認為敗血症大鼠的體內變化並無法誘發熱休克蛋白質的合成,而熱休克蛋白的大量存在下,的確可以參與敗血症的臨床表現並影響其死亡率。因此尋求一臨床上安全且可接受的誘發熱休克蛋白質合成的方法,加諸於嚴重感染的個體,應有助於改善其治療結果。 |
英文摘要 | Sepsis is an increasingly common and lethal diagnosis in hospitalized patients. In spite of the advances in antibiotics and medical equipment, the mortality rate has not been improved in the last decade. Recently, heat shock proteins(Hsps) have been well documented to play a self-protective role in almost all living cells under various pathological and physiological stresses through a mechanism known as thermotolerance or cross tolerance. The present study was designed to investigate the expression if Hsp72 and the protective role of pre-induction of Hsps in the mortality during different phases of sepsis. Adult male Sprague-Dawley rats were employed in the study. Sepsis was induced by cecal ligation and puncture (CLP). Heat shock treatment was performed 16 hrs before sepsis induction by heating the rats whole-bodily with an electric heating pad under general anesthesia. The mortality rates with time in both control and preheated groups were monitored. Hsp72 was detected by SDS-PAGE. Western blotting and immunostaining in the brain, heart, liver, kidney, lung, adrenal gland, muscle and lymphocytes. The results show that both early(9 hrs post-CLP) and late(18 hrs post-CLP) sepsis failed to increase the synthesis of Hsp72. Previous induction of Hsps by heat shock treatment significantly decreased the mortality rate of late sepsis. Applying a sufficient inducer to lymphocytes of late sepsis reversed the synthesis of Hsp72 form inactive state into an over-expressive situation in vitro. These results suggest that Hsps are involved in the pathogenesis of sepsis and the involvement of Hsps during the progression of sepsis could add to a first line of host defense against invasive pathogens. Searching for an acceptable agent or less invasive method that leads to increased Hsps expression may provide a means for better treatment of severe infection. |
本系統中英文摘要資訊取自各篇刊載內容。