Ginsenoside Rk1

Type 2 Diabetes Mellitus (T2DM) is a metabolic disease characterized by low-grade chronic inflammation in tissues such as white adipose tissue, which play a vital role in the development of insulin resistance. Ginsenoside Rk1, a minor ginsenoside derived from steamed or puffed ginseng, exhibits various pharmacological effects, including protection against endothelial dysfunction and β-cell apoptosis. However, its anti-diabetic effects remain largely unexplored.

This study investigated the anti-inflammatory and anti-diabetic effects of Ginsenoside Rk1 in bone marrow-derived macrophages (BMDMs) and high-fat diet (HFD)-induced diabetic mice, with a focus on adipose tissue inflammation.

In diabetic BMDMs and mice, we investigated whether Ginsenoside Rk1 possessed anti-diabetic and anti-inflammatory effects. We used different molecular biology techniques to study the underlying mechanisms of Ginsenoside Rk1 in mediating these effects. We also investigated the role of signal transducer and activator of transcription 3 (STAT3) in mediating the anti-inflammatory and anti-diabetic effects by using a specific STAT3 inhibitor Stattic.

Ginsenoside Rk1 exerted anti-diabetic effects in diabetic mice, evidenced by reduced fasting blood glucose levels and improved glucose tolerance and insulin resistance. These protective effects were mediated by the suppression of adipose tissue inflammation, characterized by increased interleukin-10 (IL-10) levels, decreased pro-inflammatory cytokine levels, and M2 polarization induction. These effects were also confirmed in diabetic BMDMs. The IL-10/STAT3 pathway was shown to be crucial for the alleviation of adipose tissue inflammation by Ginsenoside Rk1, with STAT3 identified as a potential direct target of Ginsenoside Rk1. STAT3 inhibition reversed the protective effects of Ginsenoside Rk1 in diabetic mice.

Our findings unveiled the remarkable anti-diabetic effects of Ginsenoside Rk1 in diabetic mice, emphasizing the pivotal role of STAT3 in alleviating adipocyte hypertrophy, adipose tissue inflammation and T2DM.

Anthracnose is a highly contagious and destructive plant disease caused by Colletotrichum gloeosporioides. The objective of this study was to investigate the antifungal activity and mechanism of ginsenoside Rk1 (GRk1) against C. gloeosporioides. In vitro experiments demonstrated that GRk1 exhibited substantial antifungal activity, with EC₅₀ values of 64.58 mg L^-1, surpassing the plant-derived pesticide d-limonene. Additionally, GRk1 could effectively suppress the dissemination of anthracnose spots in postharvest fruit. By observing the microstructure of C. gloeosporioides, it was observed that the mycelium structure underwent notable changes, and autophagosomes engulfed the organelles in the experimental groups. Fluorescent staining revealed specific signals in mycelial autophagosomes, and Western Blot analysis confirmed the upregulation of the autophagy-related protein Atg8. These findings indicate that GRk1 may activate the autophagy process by promoting Atg8 expression. Proteomic analysis revealed that the expression of Sec20 and Mpv17 proteins was significantly downregulated, whose dysregulated expression is associated with the crosstalk between SNAREs and peroxisomes during vesicle trafficking and metabolic processes. Assessment of catalase (CAT) activity, hydrogen peroxide (H₂O₂) content, and superoxide anion (O₂^-) levels further demonstrated that GRk1 could disrupt intracellular reactive oxygen species (ROS) homeostasis in mycelia. Moreover, the introduction of the ROS scavenger N-acetylcysteine (NAC) markedly inhibited autophagy, indicating that GRk1 promotes autophagy by inducing oxidative stress. Collectively, GRk1 inhibits pathogens via the ROS-autophagy axis. These findings suggested that GRk1 holds potential as a promising alternative to fungicides for the biological control of anthracnose.