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 3.9 3区 医学 Q1 MEDICAL LABORATORY TECHNOLOGY
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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来源期刊
Pharmaceutical Biology
Pharmaceutical Biology 医学-药学
CiteScore
6.70
自引率
2.60%
发文量
191
审稿时长
1 months
期刊介绍: Pharmaceutical Biology will publish manuscripts describing the discovery, methods for discovery, description, analysis characterization, and production/isolation (including sources and surveys) of biologically-active chemicals or other substances, drugs, pharmaceutical products, or preparations utilized in systems of traditional medicine. Topics may generally encompass any facet of natural product research related to pharmaceutical biology. Papers dealing with agents or topics related to natural product drugs are also appropriate (e.g., semi-synthetic derivatives). Manuscripts will be published as reviews, perspectives, regular research articles, and short communications. The primary criteria for acceptance and publication are scientific rigor and potential to advance the field.
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