Sodium Butyrate Ameliorates l-Arginine-Induced Pancreatitis and Associated Fibrosis in Wistar Rat: Role of Inflammation and Nitrosative Stress
Sodium Butyrate Ameliorates l-Arginine-Induced Pancreatitis and Associated Fibrosis in Wistar Rat: Role of Inflammation and Nitrosative Stress
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DOI：
10.1002/jbt.21698
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发表时间：
2015-08-01
影响因子：
3.6
通讯作者：
Jena, Gopabandhu
中科院分区：
文献类型：
--
作者：
Kanika, Gayathri;Khan, Sabbir;Jena, Gopabandhu
一些报道表明组蛋白去乙酰化酶（HDAC）在炎症和纤维化中起关键作用。丁酸钠（SB）是一种具有HDAC抑制潜力的短链脂肪酸。本研究旨在评价SB对l-精氨酸（l-Arg）诱导的Wistar大鼠胰腺纤维化的保护作用。通过两次腹膜内（i. p.）在第1、4、7和10天每隔2小时注射20% l-Arg（250 mg/100 g），而SB（800 mg/kg/天）给药10天。在研究结束时，对生化评估、组织学改变、DNA损伤和各种蛋白质的表达进行了评价。SB的后处理降低了l-Arg诱导的氧化和亚硝化应激，DNA损伤，组织学改变和纤维化。有趣的是，SB后处理显著降低了β-平滑肌肌动蛋白，白细胞介素-1，诱导型一氧化氮合酶和3-硝基酪氨酸的表达。本研究表明SB后处理可减轻l-Arg诱导的大鼠胰腺损伤和纤维化。
Several reports indicated that histone deacetylases (HDACs) play a crucial role in inflammation and fibrogenesis. Sodium butyrate (SB) is a short-chain fatty acid having HDAC inhibition potential. The present study aimed to evaluate the protective effect of SB against l-arginine (l-Arg)-induced pancreatic fibrosis in Wistar rats. Pancreatic fibrosis was induced by twice intraperitoneal (i.p.) injections of 20% l-Arg (250 mg/100 g) at 2-h interval on day 1, 4, 7, and 10, whereas SB (800 mg/kg/day) was administrated for 10 days. At the end of the study, biochemical estimations, histological alterations, DNA damage, and the expression of various proteins were evaluated. Posttreatment of SB decreased l-Arg-induced oxidative and nitrosative stress, DNA damage, histological alterations, and fibrosis. Interestingly, posttreatment of SB significantly decreased the expression of -smooth muscle actin, interleukin-1, inducible nitric oxide synthase, and 3-nitrotyrosine. The present study demonstrated that posttreatment of SB alleviates l-Arg-induced pancreatic damage and fibrosis in rat.