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

• Published in: Pharmaceutical biology Vol. 60; no. 1; pp. 2229 - 2236
• Main Authors: Su, Hao, Tian, Cheng-Ju, Wang, Ying, Shi, Jiaojiao, Chen, Xiaoxiao, Zhen, Zhong, Bai, Yu, Deng, Lan, Feng, Chunpeng, Ma, Zhuang, Liu, Jinfeng
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01.12.2022; Taylor & Francis Ltd; Taylor & Francis Group
• Subjects: Animals; Apoptosis; Biological activity; Diabetes; Diabetes mellitus; Diabetes Mellitus, Experimental - chemically induced; Diabetes Mellitus, Experimental - drug therapy; Diabetic lung; Ginseng; Ginsenosides; Ginsenosides - pharmacology; Inflammation; Inflammation - drug therapy; Insulin; Interleukin 1; Interleukin 6; Lung; lung injury; Lungs; Male; Oxidative Stress; Panax - chemistry; Panax ginseng; proinflammatory cytokines; Rats; Rats, Sprague-Dawley; Streptozocin; Superoxide Dismutase; Transforming Growth Factor beta; Transforming growth factor-b; Tumor Necrosis Factor-alpha; Tumor necrosis factor-α; Ultrastructure; Diabetic lung; apoptosis; proinflammatory cytokines; lung injury
• ISSN: 1388-0209; 1744-5116
• DOI: 10.1080/13880209.2022.2140168

Ginsenoside Rb1 (Rb1) is a biologically active component of ginseng [Panax ginseng C.A. Meyer (Araliaceae)]. This study determined the underlying mechanisms of Rb1 treatment that acted on diabetes-injured lungs in diabetic rats. 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. 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. These findings indicate that Rb1 could be useful for mitigating oxidative damage and inflammatory infiltration in the diabetic lung.