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Abstract Title:

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

Abstract Source:

Pharm Biol. 2022 Dec ;60(1):2229-2236. PMID: 36367996

Abstract Author(s):

Hao Su, Cheng-Ju Tian, Ying Wang, Jiaojiao Shi, Xiaoxiao Chen, Zhong Zhen, Yu Bai, Lan Deng, Chunpeng Feng, Zhuang Ma, Jinfeng Liu

Article Affiliation:

Hao Su

Abstract:

CONTEXT: Ginsenoside Rb1 (Rb1) is a biologically active component of 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 ( = 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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