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富氢生理盐水可改善大鼠 l-精氨酸诱导的急性胰腺炎的严重程度。

Hydrogen-rich saline ameliorates the severity of l-arginine-induced acute pancreatitis in rats.

机构信息

Department of General Surgery, Shanghai Chang Zheng Hospital, Second Military Medical University, PR China.

出版信息

Biochem Biophys Res Commun. 2010 Mar 5;393(2):308-13. doi: 10.1016/j.bbrc.2010.02.005. Epub 2010 Feb 6.

Abstract

Molecular hydrogen, which reacts with the hydroxyl radical, has been considered as a novel antioxidant. Here, we evaluated the protective effects of hydrogen-rich saline on the l-arginine (l-Arg)-induced acute pancreatitis (AP). AP was induced in Sprague-Dawley rats by giving two intraperitoneal injections of l-Arg, each at concentrations of 250mg/100g body weight, with an interval of 1h. Hydrogen-rich saline (>0.6mM, 6ml/kg) or saline (6ml/kg) was administered, respectively, via tail vein 15min after each l-Arg administration. Severity of AP was assessed by analysis of serum amylase activity, pancreatic water content and histology. Samples of pancreas were taken for measuring malondialdehyde and myeloperoxidase. Apoptosis in pancreatic acinar cell was determined with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling technique (TUNEL). Expression of proliferating cell nuclear antigen (PCNA) and nuclear factor kappa B (NF-kappaB) were detected with immunohistochemistry. Hydrogen-rich saline treatment significantly attenuated the severity of l-Arg-induced AP by ameliorating the increased serum amylase activity, inhibiting neutrophil infiltration, lipid oxidation and pancreatic tissue edema. Moreover, hydrogen-rich saline treatment could promote acinar cell proliferation, inhibit apoptosis and NF-kappaB activation. These results indicate that hydrogen treatment has a protective effect against AP, and the effect is possibly due to its ability to inhibit oxidative stress, apoptosis, NF-kappaB activation and to promote acinar cell proliferation.

摘要

分子氢与羟自由基反应,被认为是一种新型抗氧化剂。在这里,我们评估了富氢生理盐水对 l-精氨酸(l-Arg)诱导的急性胰腺炎(AP)的保护作用。通过给 Sprague-Dawley 大鼠腹腔内注射两次 l-Arg,每次浓度为 250mg/100g 体重,间隔 1h,诱导 AP。分别在两次 l-Arg 注射后 15min 通过尾静脉给予富氢生理盐水(>0.6mM,6ml/kg)或生理盐水(6ml/kg)。通过分析血清淀粉酶活性、胰腺含水量和组织学来评估 AP 的严重程度。取胰腺样本测量丙二醛和髓过氧化物酶。用末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记技术(TUNEL)测定胰腺腺泡细胞凋亡。用免疫组织化学法检测增殖细胞核抗原(PCNA)和核因子 kappa B(NF-kappaB)的表达。富氢盐水治疗通过改善血清淀粉酶活性的升高、抑制中性粒细胞浸润、脂质氧化和胰腺组织水肿,显著减轻了 l-Arg 诱导的 AP 的严重程度。此外,富氢盐水治疗可以促进腺泡细胞增殖,抑制细胞凋亡和 NF-kappaB 激活。这些结果表明,氢气处理对 AP 具有保护作用,其作用可能是由于其抑制氧化应激、细胞凋亡、NF-kappaB 激活和促进腺泡细胞增殖的能力。

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