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.
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人参皂苷 Rb1 减少链脲佐菌素诱导的糖尿病大鼠的氧化/羰基应激损伤并改善肺部炎症

DOI:
10.1080/13880209.2022.2140168
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发表时间:
2022-12
影响因子:
3.8
通讯作者:
Liu, Jinfeng
Liu, Jinfeng
中科院分区:
医学3区
文献类型:
--
作者:
Su, Hao;Tian, Cheng-Ju;Wang, Ying;Shi, Jiaojiao;Chen, Xiaoxiao;Zhen, Zhong;Bai, Yu;Deng, Lan;Feng, Chunpeng;Ma, Zhuang;Liu, Jinfeng

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摘要 背景 人参皂苷 Rb1 (Rb1) 是人参 [Panax ginseng C.A.梅耶(五加科)]。目的 本研究确定 Rb1 治疗对糖尿病大鼠糖尿病损伤肺部的潜在机制。材料和方法使用链脲佐菌素(STZ)诱导的糖尿病大鼠模型。雄性Sprague-Dawley (SD)大鼠被分为四组(n = 10):对照组、Rb1(20mg/kg)、胰岛素(15U/kg以达到血糖正常状态)和糖尿病组(未治疗)。治疗六周后,氧化应激测定;组织学和超微结构分析; TNF-α、TGF-β、IL-1和IL-6蛋白表达分析;并进行细胞凋亡检测。结果糖尿病组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治疗增加了SOD(2.4倍)、CAT(1.9倍)和GSH(1.29倍),并降低了NO(1.76倍)和MDA(1.51倍)水平。糖尿病大鼠中IL-6(5.13倍)、IL-1α(2.35倍)、TNF-α(2.35倍)和TGF-β(2.39倍)的表达较对照组增加。 Rb1治疗组中IL-6(2.43倍)、IL-1α(2.27倍)、TNF-α(1.68倍)和TGF-β(2.3倍)降低。糖尿病增加了细胞凋亡率(与对照组相比为2.23倍),而Rb1治疗降低了细胞凋亡率(与糖尿病大鼠相比为1.73倍)。 Rb1 和胰岛素可改善肺组织损伤。讨论和结论这些研究结果表明,Rb1 可用于减轻糖尿病肺部的氧化损伤和炎症浸润。
Abstract 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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