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番茄红素对急性胰腺炎中诱导型一氧化氮合酶和肿瘤坏死因子-α水平的抑制作用与甲泼尼龙相当。

Suppression of inducible nitric oxide synthase and tumor necrosis factor-alpha level by lycopene is comparable to methylprednisolone in acute pancreatitis.

机构信息

Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, El-Gharbia, Egypt.

出版信息

Dig Liver Dis. 2018 Jun;50(6):601-607. doi: 10.1016/j.dld.2018.01.131. Epub 2018 Feb 2.

Abstract

BACKGROUND

Oxidative stress and inflammation may play a key role in the pathogenesis of acute pancreatitis (AP). Lycopene, a natural carotenoid, has antioxidant scavenger capacity and inhibits inflammation in many experimental models.

AIM

The study was designed to investigate whether lycopene can ameliorate l-arginine-induced pancreatitis in rats and to elucidate the underlying molecular mechanisms of these effects.

METHODS

Forty-eight adult male Wistar rats were divided into: control group (vehicle, orally, 10 days), AP group (3 g/kg l-arginine, single i.p. injection, on day 10th of the experiment), lycopene group (50 mg/kg) and methylprednisolone group (30 mg/kg). Lycopene and methylprednisolone were given orally, once daily for 10 days prior to l-arginine injection. Rats were sacrificed 24 h after l-arginine injection. Inflammation/oxidative stress and pancreatic markers were assessed. Pancreatic histopathological studies were done.

RESULTS

Lycopene group showed a significant reduction in tumor necrosis factor alpha (TNF-α), myeloperoxidase activity, and down-regulation of inducible nitric oxide synthase (iNOS) gene expression. Pancreatic nitric oxide concentration was reduced and pancreatic GSH was increased in lycopene group. Serum α-amylase and lipase activities were reduced by lycopene treatment. The histology of pancreas was improved in lycopene group as well as methylprednisolone group.

CONCLUSION

Lycopene prior treatment proved anti-inflammatory and antioxidant effects against AP rat model via different mechanisms.

摘要

背景

氧化应激和炎症可能在急性胰腺炎(AP)的发病机制中起关键作用。番茄红素是一种天然类胡萝卜素,具有抗氧化清除能力,并在许多实验模型中抑制炎症。

目的

本研究旨在探讨番茄红素是否可以改善大鼠的精氨酸诱导的胰腺炎,并阐明这些作用的潜在分子机制。

方法

将 48 只成年雄性 Wistar 大鼠分为:对照组(载体,口服,10 天)、AP 组(3g/kg 精氨酸,单次腹腔注射,实验第 10 天)、番茄红素组(50mg/kg)和甲泼尼龙组(30mg/kg)。番茄红素和甲泼尼龙在精氨酸注射前 10 天每天口服一次,共 10 天。大鼠在精氨酸注射后 24 小时处死。评估炎症/氧化应激和胰腺标志物。进行胰腺组织病理学研究。

结果

番茄红素组肿瘤坏死因子-α(TNF-α)、髓过氧化物酶活性显著降低,诱导型一氧化氮合酶(iNOS)基因表达下调。番茄红素组降低了胰腺中一氧化氮的浓度,增加了 GSH。番茄红素治疗可降低血清α-淀粉酶和脂肪酶的活性。番茄红素组和甲泼尼龙组的胰腺组织学均得到改善。

结论

番茄红素预处理对 AP 大鼠模型具有抗炎和抗氧化作用,其作用机制不同。

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