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Ascitic fluid and serum from rats with acute pancreatitis injure rat pancreatic tissues and alter the expression of heat shock protein 60

机译:急性胰腺炎大鼠腹水和血清损伤大鼠胰腺组织并改变热休克蛋白60的表达

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Acute pancreatitis (AP) is an inflammatory process in which cytokines and chemokines are involved. After onset, extrapancreatic stimuli can induce the expression of cytokines in pancreatic acinar cells, thereby amplifying this inflammatory loop. To further determine the role and mechanism of irritating agents in the pathogenesis of AP, rat pancreatic tissues were stimulated with ascitic fluid (APa) and serum (APs) from rats with AP or with lipopolysaccharide (LPS). In addition, the alteration of heat shock protein 60 (HSP60) expression was evaluated. Rat pancreas was removed and meticulously snipped to fragments. The snips were cultured for up to 48?h. During this period, the tissue viability as well as amylase and TNF-α levels in the supernatant and the HSP60 expression in the pancreatic tissue before and after stimulation by APa, APs, and LPS were assayed time-dependently. At different time-points during the culture, the viability and the amylase activity in the pancreatic tissue remained largely stable. After stimulation with APa, APs, or LPS for 1?h, the pancreatic tissues showed some damage, and this was followed by a sharp decrease in the viability accompanied by increased levels of amylase and TNF-α in the culture medium 2 or 4?h after stimulation (p?
机译:急性胰腺炎(AP)是一种炎症过程,其中涉及细胞因子和趋化因子。发病后,胰腺外刺激可诱导胰腺腺泡细胞中细胞因子的表达,从而放大这种炎症环。为了进一步确定刺激物在AP发病机理中的作用和机制,用腹水(APa)和来自患有AP或脂多糖(LPS)的大鼠的血清(AP)刺激大鼠胰腺组织。此外,评估了热激蛋白60(HSP60)表达的变化。取出大鼠胰腺,并小心地将其剪成碎片。剪培养到48?h。在此期间,通过时间依赖性地分析了在被APa,AP和LPS刺激之前和之后,上清液中的组织活力以及淀粉酶和TNF-α水平以及胰腺组织中HSP60的表达。在培养期间的不同时间点,胰腺组织中的活力和淀粉酶活性基本保持稳定。在用APa,AP或LPS刺激1?h后,胰腺组织显示出一定程度的损伤,随后活力急剧下降,同时培养基2或4?中淀粉酶和TNF-α的水平升高。刺激后h(p≤0.05)。相反,HSP60 mRNA和蛋白质水平在新鲜制备的组织片段中均具有相对较高的表达(0?h)。随着培养时间的延长,HSP60 mRNA的表达仅略有下降。同时,HSP60蛋白水平在延长的培养时间内降低,从12到48?h明显降低(p 0.05)。用AP,APa或LPS刺激后,组织片段中HSP60 mRNA和蛋白的表达在1?h略有增加,而在2和4?h则显着下降(p <0.05)。 APa,AP或LPS在孤立的胰腺组织上引起损伤,并伴随着HSP60表达模式的变化,并呈时间依赖性。

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