N-acetylcysteine protects against acute pancreatitis in rats

doi:10.3969/j.issn.2095-4344.2015.05.018

Abstract

Abstract:

BACKGROUND: Acute pancreatitis is a common inflammatory disease mediated by pancreatic acinar cells injury, and is mainly characterized by leukocyte infiltration. N-acetylcysteine can control leukocyte migration and regulate inflammation in some serious inflammatory diseases.
OBJECTIVE: To investigate the protective effects of N-acetylcysteine in rat model of acute pancreatitis caused by sodium taurocholate.
METHODS: Ninety Sprague-Dawley rats were randomly divided into three groups: normal control group, acute pancreatitis group and N-acetylcysteine group. Except normal control group, acute pancreatitis model was established in the other two groups by retrograde injection of sodium taurocholate into major duodenal papilla. Rats in the N-acetylcysteine group were treated with N-acetylcysteine intravenously through the tail vein.
RESULTS AND CONCLUSION: After acute pancreatitis model was established, plasma amylase levels in the models were significantly higher than that in the normal control rats (P < 0.05). Interleukin-1β, -6, -10, and tumor necrosis factor α expression levels were also obviously higher than that in the normal control rats (P < 0.05). Immunohistochemical staining demonstrated that N-acetylcysteine was mainly expressed in the islet cells, and the pancreatic expression of N-acetylcysteine was down-regulated at both the mRNA and protein levels during the course of acute pancreatitis. N-acetylcysteine administration significantly reduced plasma amylase levels, myeloperoxidase activity, pro-inflammatory cytokine production, and pancreas and lung tissue damages. Furthermore, N-acetylcysteine administration did not cause significant inhibition of nuclear factor-κB activation in the pancreas. N-acetylcysteine is capable of improving damage of pancreas and lung, and exerting anti-inflammatory effects in rats with severe acute pancreatitis.

中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程

全文链接：

Key words: Pancreatitis, Inflammation, Interleukins, Pancreatic Islet

CLC Number:

R318

Meng Xian-pu, Yan Wen-zhu, Shan Wei. N-acetylcysteine protects against acute pancreatitis in rats[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(5): 759-765.

Figures/Tables 5

2.3 N-乙酰半胱氨酸对急性胰腺炎大鼠血清淀粉酶水平的影响血浆淀粉酶升高是胰腺泡心细胞损伤的重要标志。急性胰腺炎模型诱导后的24，48，72和96 h后血浆淀粉酶活性较正常对照组大鼠显著升高(P < 0.05)。N-乙酰半胱氨酸治疗分别在24，48，72和96 h较急性胰腺炎组显著的降低了血浆淀粉酶水平(P < 0.05；图2A)。 2.4 N-乙酰半胱氨酸对急性胰腺炎大鼠胰腺组织髓过氧化物酶和组织病理变化的影响胰腺组织中髓过氧化物酶活性随着急性胰腺炎的进展显著增加，在急性胰腺炎模型成功后的72 h达到高峰，与血浆淀粉酶水平的最高峰在同一时间点上(P < 0.05；图2B)。N-乙酰半胱氨酸治疗于48，72和96 h后较急性胰腺炎组髓过氧化物酶活性显著降低(P < 0.05；图2B)。胰腺组织苏木精-伊红染色切片组织学评估显示，随着急性胰腺炎诱导成功后时间变化胰腺组织出现损伤，而正常对照组动物胰腺组织未见任何改变。在模型诱导后0 h，急性胰腺炎组和N-乙酰半胱氨酸组胰腺的组织学结构和特征都是正常的。大鼠急性胰腺炎后胰腺组织开始出现水肿，中性粒细胞浸润，出血，泡心细胞坏死等现象，于 72 h达到峰值，然而在胰岛处未出现形态学改变。与急性胰腺炎组相比胰腺组织水肿，中性粒细胞浸润，出血，泡心细胞坏死以及总组织学评分在N-乙酰半胱氨酸治疗后显著降低(P < 0.05；图2C，D)。 N-乙酰半胱氨酸对急性胰腺炎大鼠肺组织髓过氧化物酶活性和组织学影响之前的研究结果相似，急性胰腺炎动物同时伴有肺的损伤。图3A显示，当动物被诱导成急性胰腺炎后肺髓过氧化物酶活性显著增加，72 h时达到峰值。与急性胰腺炎组相比，N-乙酰半胱氨酸治疗能在24，48，72和96 h显著降低髓过氧化物酶活性(P < 0.05)。通过组织学观察更加证明了肺的损伤情况，肺组织出现了大量炎性细胞的浸润，肺水肿，肺泡和间质出血。损伤最严重也发生在急性胰腺炎后的72 h。N-乙酰半胱氨酸治疗后明显的降低了炎性细胞的浸润，肺水肿，出血以及肺的组织学总评分(P < 0.05；图3B，C)。"

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