消化道的上皮組織在正常情況下，是藉由緻密接合所連接，可做為結構性的保護屏障及細胞間的通道，當發炎反應發生時，發炎組織的微循環系統會有血管滲透性增加的現象，造成血漿滲漏。同時，在哺乳類的腸道上皮組織存在有許多的杯狀細胞，在發炎的情況下會排放黏液，其分泌的黏液主要的功能是保護及潤滑小腸內腔，被視為抵抗腸道細菌入侵，物理性傷害與化學性刺激物的第一道防線。熱休克反應是最原始的細胞防禦機制之一，生物體在種種的壓力情況，包括環境的（紫外線輻射或重金屬），病理的（感染或惡性腫瘤），生理的（生長因子）刺激下會誘發熱休克蛋白產生。
本實驗使用兩種不同品系的大鼠作為實驗對象，探討熱休克反應對內毒素所誘發的血漿滲漏與杯狀細胞的黏液排放有何影響。利用印地安墨汁當追蹤劑，標定發炎血漿滲漏的血管。小腸絨毛表面杯狀細胞黏液分泌的情形則利用掃描式電子顯微鏡觀察，並使用數位影像分析軟體 (SimplePCI, Compix, Inc.) 進行計量分析。實驗結果顯示，注射內毒素之實驗組相較於注射生理食鹽水之對照組，在兩個品系皆明顯的引起血漿滲漏並增加杯狀細胞黏液的排放。杯狀細胞進行複合胞吐作用排放出黏液顆粒後，在小腸絨毛表面可觀察到許多的孔洞。LE品系大鼠予以熱休克前處理，可以抑制內毒素注射後30分鐘或1小時所誘發的小腸血漿滲漏現象達到58-80％(P <0.01)；而在內毒素注射後1小時，可以減少內毒素所誘發的迴腸杯狀細胞黏液排放(P <0.05)。SD品系大鼠予以熱休克前處理，可以抑制內毒素注射後1小時所誘發的小腸血漿滲漏現象達到56-68％(P<0.01)，以及減少十二指腸和迴腸杯狀細胞黏液排放(P <0.05)。由實驗結果推論，對內毒素所誘發的發炎與黏液排放現象，熱休克反應可以達到保護大鼠腸道的作用。

The gastrointestinal epithelium normally sealed by tight junctions, which act as a structural barrier and paracellular channels. Inflammation can increase the permeability of microvasculature that result in plasma leakage. Mammalian intestinal epithelium has many goblet cells which discharge mucus in the inflammatory response. The discharging mucus functioning is as a defensive barrier and lubricant. The mucus layer is the anatomical site at which the host first encounters gut bacteria, physical damage, and chemical stimulant. The heat shock response is one of the most primitive cellular defense mechanism. A variety of stressful situations including environmental (ultraviolet radiation or heavy metals), pathological (infections or malignancies), or physiological (growth factors) stimuli induce heat shock proteins.
This study investigated the effect of heat shock on endotoxin-induced plasma leakage and goblet cell mucus discharge in the small intestine of rats of Sprague-Dawley (SD) and Long-Evans (LE) strains. India ink was used as the tracer to detect leaky microvessels. The mucus secretion of the goblet cells of intestinal villi was observed with scanning electron microscopy and calculated with digital morphomertric software SimplePCI. Our results showed that endotoxin-induced plasma leakage and goblet cell discharging in the two strains increased significantly as compared to rat groups receiving saline. Numerous openings on the epithelial surface of villi resulted from compound exocytosis of mucus granules in goblet cells. Either 30 min or 1h after LPS injection, heat shock pretreatment in LE rats LPS-induced plasma leakage in the duodenum and ileum was reduced by 58-80% (P<0.01). 1 h after LPS injection in LE rats pretreated with heat shock, the number of discharging goblet cells in the ileum was reduced (P<0.05). In SD rats, heat shock inhibited LPS-induced plasma leakage in the duodenum and ileum at 1h after LPS injection by 56-68% (P<0.01), and the number of discharging goblet cells was reduced in the duodenum and ileum (P<0.05). In conclusion, heat shock could protect rat intestine from endotoxin-induced inflammation and mucus secretion.

【中文摘要】--------------------------------------------------------------------2
【Abstract】----------------------------------------------------------------------4
【緒論】--------------------------------------------------------------------------6
【研究目的】-------------------------------------------------------------------14
【實驗流程】-------------------------------------------------------------------15
【材料與方法】----------------------------------------------------------------16
【實驗結果】-------------------------------------------------------------------23
【討論】-------------------------------------------------------------------------31
【結論】-------------------------------------------------------------------------36
【參考文獻】-------------------------------------------------------------------37
【圖及圖解】-------------------------------------------------------------------44

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