Why the study?
Does ginsenoside treatment improve metabolic and angiopathy markers in diabetic Wistar rats?
Does ginsenoside treatment improve metabolic and angiopathy markers in diabetic Wistar rats?
Ginsenoside Re demonstrates protective and anti-angiopathy effects in diabetic rat models, potentially via modulation of p38 MAPK, ERK1/2, and JNK signaling pathways.
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Supports GSS protective effects in diabetic rat models; leaves open human translation pending clinical trials.
The present study aimed to determine the protective and anti-angiopathy effects of ginsenoside (GSS) on Wistar rats with diabetes mellitus (DM). Diabetic angiopathy occurs during the early stage of diabetes, and in type 1 DM (T1DM) and type 2 DM (T2DM). In the present study, early DM, T1DM and T2DM were induced by treatment with a high‑sucrose‑high‑fat diet, alloxan monohydrate or streptozocin, respectively. The levels of blood glucose, insulin, lipid metabolism markers [total cholesterol (TC), triglyceride (TG), high‑density lipoprotein (HDL) and lipoprotein(a) (Lp‑a)], and endothelial cell function markers [endothelin, nitric oxide, vascular endothelial growth factor (VEGF) and interleukin‑6 (IL‑6)] were determined following treatment with GSS. In addition, oral glucose tolerance test and insulin tolerance test were performed. The phosphorylation levels of p38 mitogen‑activated protein kinase (MAPK), extracellular signal‑regulated kinase 1/2 (ERK1/2) and c‑Jun N‑terminal kinase (JNK) were detected in aorta samples harvested from T2DM rats by western blot analysis. The present study determined that GSS treatment effectively decreased the levels of blood glucose, TC, TG, Lp‑a, VEGF, IL‑6, phosphorylated (p)‑p38, p‑ERK1/2 and p‑JNK; however, treatment with GSS increased insulin and HDL levels. Therefore, it is possible that GSS exerts protective and anti‑angiopathy effects against the early stage of diabetes, T1DM and T2DM in vivo via the activation of p38 MAPK, ERK1/2 and JNK signaling.
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Shi et al. (2016) studied this question.
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