人参皂苷Rb1减轻链脲佐菌素诱导的糖尿病大鼠的氧化/羰基应激损伤,改善肺部炎症。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Hao Su, Cheng-Ju Tian, Ying Wang, Jiaojiao Shi, Xiaoxiao Chen, Zhong Zhen, Yu Bai, Lan Deng, Chunpeng Feng, Zhuang Ma, Jinfeng Liu
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引用次数: 1

摘要

背景:人参皂苷Rb1 (Rb1)是人参的一种生物活性成分[Panax ginseng C.A. Meyer (Araliaceae)]。目的:探讨Rb1对糖尿病大鼠肺损伤的作用机制。材料与方法:采用链脲佐菌素(STZ)诱导的糖尿病大鼠模型。雄性Sprague-Dawley (SD)大鼠分为4组(n = 10):对照组、Rb1组(20 mg/kg)、胰岛素组(15 U/kg达到血糖状态)和糖尿病组(未经治疗)。治疗6周后进行氧化应激测定;组织和超微结构分析;TNF-α、TGF-β、IL-1、IL-6蛋白表达分析;并进行细胞凋亡检测。结果:糖尿病组与对照组相比,SOD(3.53倍)、CAT(2.55倍)、GSH(1.63倍)活性降低,NO(4.47倍)、MDA(3.86倍)水平升高。与糖尿病大鼠相比,Rb1处理使SOD(2.4倍)、CAT(1.9倍)和GSH(1.29倍)升高,使NO(1.76倍)和MDA(1.51倍)降低。与对照组相比,糖尿病大鼠IL-6(5.13倍)、IL-1α(2.35倍)、TNF-α(2.35倍)、TGF-β(2.39倍)表达增加。Rb1治疗组IL-6(2.43倍)、IL-1α(2.27倍)、TNF-α(1.68倍)、TGF-β(2.3倍)降低。糖尿病组大鼠细胞凋亡率升高(比对照组高2.23倍),Rb1组大鼠细胞凋亡率降低(比糖尿病组低1.73倍)。Rb1和胰岛素可改善肺组织损伤。讨论和结论:这些发现表明Rb1可能有助于减轻糖尿病肺的氧化损伤和炎症浸润。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ginsenoside Rb1 reduces oxidative/carbonyl stress damage and ameliorates inflammation in the lung of streptozotocin-induced diabetic rats.

Ginsenoside Rb1 reduces oxidative/carbonyl stress damage and ameliorates inflammation in the lung of streptozotocin-induced diabetic rats.

Ginsenoside Rb1 reduces oxidative/carbonyl stress damage and ameliorates inflammation in the lung of streptozotocin-induced diabetic rats.

Ginsenoside Rb1 reduces oxidative/carbonyl stress damage and ameliorates inflammation in the lung of streptozotocin-induced diabetic rats.

Context: Ginsenoside Rb1 (Rb1) is a biologically active component of ginseng [Panax ginseng C.A. Meyer (Araliaceae)].

Objective: This study determined the underlying mechanisms of Rb1 treatment that acted on diabetes-injured lungs in diabetic rats.

Materials and methods: Streptozotocin (STZ)-induced diabetic rat model was used. Male Sprague-Dawley (SD) rats were divided into four groups (n = 10): control, Rb1 (20 mg/kg), insulin (15 U/kg to attain the euglycaemic state) and diabetic (untreated). After treatment for six weeks, oxidative stress assay; histological and ultrastructure analyses; TNF-α, TGF-β, IL-1 and IL-6 protein expression analyses; and the detection of apoptosis were performed.

Results: There was decreased activity of SOD (3.53-fold), CAT (2.55-fold) and GSH (1.63-fold) and increased levels of NO (4.47-fold) and MDA (3.86-fold) in the diabetic group from control. Rb1 treatment increased SOD (2.4-fold), CAT (1.9-fold) and GSH (1.29-fold) and decreased the levels of NO (1.76-fold) and MDA (1.51-fold) as compared with diabetic rats. The expression of IL-6 (5.13-fold), IL-1α (2.35-fold), TNF-α (2.35-fold) and TGF-β (2.39-fold) was increased in diabetic rats from control. IL-6 (2.43-fold), IL-1α (2.27-fold), TNF-α (1.68-fold) and TGF-β (2.3-fold) were decreased in the Rb1 treatment group. Diabetes increased the apoptosis rate (2.23-fold vs. control), and Rb1 treatment decreased the apoptosis rate (1.73-fold vs. the diabetic rats). Rb1 and insulin ameliorated lung tissue injury.

Discussion and conclusions: These findings indicate that Rb1 could be useful for mitigating oxidative damage and inflammatory infiltration in the diabetic lung.

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