【摘要】：急性胰腺炎(Acute pacreatitis,AP)是一種常見的臨床急性腹部疾病,近年來發(fā)病率持續(xù)升高,但市場上尚未有治療AP的特效藥。與AP相關的腸道損傷將反過來加重的病情惡化。此研究旨在探究一種提取自檸檬的低酯果膠(Low-methoxyl pectin,LMP)是否可以減輕AP嚴重程度及其相關腸黏膜屏障損傷。本研究將BALB/c小鼠隨機分成正常對照組、急性胰腺炎模型組、低酯果膠組,通過雨蛙素(Caerulein,CAE)過度刺激誘導AP模型,收取血清、胰腺、結腸、回腸等樣品。通過測定小鼠血清淀粉酶水平、血清脂肪酶水平、胰腺髓過氧化物酶活力、胰腺水腫程度研究低酯果膠是否能夠減輕急性胰腺炎嚴重程度;通過測定血清及胰腺中TNF-α、IL-1β及IL-6的水平研究低酯果膠是否可以降低AP病程中炎癥因子的分泌;通過測定血清內毒素含量,腸道中緊密連接蛋白ZO-1及Occuldin和抗菌肽DEFB1及CRAMP的表達水平,小鼠糞便中短鏈脂肪酸水平研究低酯果膠是否可以保障AP小鼠腸道屏障功能;通過測定腸道中TNF-α、IL-1β及IL-6的水平研究低酯果膠是否可以減輕AP小鼠腸道炎癥反應。實驗結果發(fā)現(xiàn)膳食補充低酯果膠后,小鼠的AP嚴重程度降低,表現(xiàn)為血清淀粉酶及脂肪酶水平,胰腺水腫程度及髓過氧化物酶活性的降低。胰腺組織病理切片的組織學檢查也證實了低酯果膠的保護作用。膳食補充低酯果膠還可以抑制胰腺中促炎細胞因子的分泌,包括TNF-α,IL-1β和IL-6。此外,膳食補充低酯果膠恢復了AP相關腸道屏障的損傷,如上調了腸道緊密連接蛋白Occludin及ZO-1和抗菌肽DEFB1及Cramp的表達,增加了小鼠腸道短鏈脂肪酸的產量。并且,與CAE組相比,膳食補充了低酯果膠的AP小鼠表現(xiàn)出腸道炎癥反應被抑制,結腸及回腸的促炎細胞因子分泌減少。綜上,低酯果膠可以通過保障腸道屏障功能從而減輕小鼠AP的嚴重程度。本研究的實驗結果表明,低酯果膠可作為有效的營養(yǎng)干預手段減輕AP的嚴重程度及相關腸道屏障損傷。該保護作用的機制可能跟低酯果膠的炎癥抑制與腸道黏膜屏障功能的保護作用有關。低酯果膠作為一種安全健康的可溶性膳食纖維,或許可將其開發(fā)成AP相關功能性食品,以更好地預防、緩解AP。
[Abstract]:Acute pancreatitis (AP) is a common clinical acute abdominal disease, the incidence of which has been increasing in recent years, but there is no specific drug to treat AP in the market. Intestinal injury associated with AP will in turn worsen the condition. The aim of this study was to investigate whether a Low-methoxyl pectin extracted from lemon can reduce the severity of AP and its associated intestinal mucosal barrier damage. In this study, BALB/c mice were randomly divided into normal control group, acute pancreatitis model group and low-ester pectin group. AP model was induced by excessive stimulation of Caerulein (CAE). Serum, pancreas, colon and ileum were collected. The levels of serum amylase, serum lipase, the activity of pancreatic myeloperoxidase and the degree of pancreatic edema were measured to study whether low ester pectin could reduce the severity of acute pancreatitis. To study whether low ester pectin can reduce the secretion of inflammatory factors in the course of AP, to determine the levels of TNF- 偽 -IL-1 尾 and IL-6 in serum and pancreas, and to determine the expression of ZO-1, Occuldin, DEFB1 and CRAMP in intestinal tract by measuring the content of endotoxin in serum. Effects of low Ester Pectin on intestinal Barrier function in AP mice and the effects of low Ester Pectin on intestinal inflammation in AP mice were studied by measuring the levels of TNF- 偽 -TNF- 偽 -IL-1 尾 and IL-6. The results showed that the severity of AP in mice decreased after dietary supplementation of low ester pectin, including the decrease of serum amylase and lipase levels, pancreatic edema and myeloperoxidase activity. Histological examination of pancreatic histopathological sections also confirmed the protective effect of low-ester pectin. Dietary supplementation of low ester pectin also inhibited the secretion of pro-inflammatory cytokines, including TNF- 偽, IL-1 尾 and IL-6. In addition, dietary supplementation of low-ester pectin restored the injury of the intestinal barrier associated with AP, such as up-regulating the expression of Occludin and ZO-1, DEFB1 and Cramp, and increasing the production of short-chain fatty acids in the intestinal tract of mice. In addition, compared with CAE group, AP mice fed with low-ester pectin diet showed inhibition of intestinal inflammatory response and decreased secretion of inflammatory cytokines in colon and ileum. In conclusion, low-ester pectin can reduce the severity of AP by protecting intestinal barrier function in mice. The results showed that low ester pectin could be used as an effective nutritional intervention to alleviate the severity of AP and related intestinal barrier damage. The protective mechanism may be related to the inflammatory inhibition of low-ester pectin and the protective effect of intestinal mucosal barrier function. As a safe and healthy soluble dietary fiber, low ester pectin may be developed into AP related functional food for better prevention and relief of APs.
【學位授予單位】：江南大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R576;TS201.4

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