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20(S)-ginsenoside Rh1 alleviates T2DM induced liver injury via the Akt/FOXO1 pathway
Wen-Ya Su1, Mei-Ling Fan2, Ying Li1
1College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
Abstract:
Diabetes-associated liver injury becomes a dominant hepatopathy, leading to hepatic failure worldwide. The current study was designed to evaluate the ameliorative effects of ginsenoside Rh1 (G-Rh1) on liver injury induced by T2DM. A T2DM model was established using C57BL/6 mice through feeding with HFD followed by injection with streptozotocin at 100 mg·kg-1.. Then the mice were continuously administered with G-Rh1 (5 and 10 mg·kg-1), to explore the protective effects of G-Rh1 against liver injury. Results showed that G-Rh1 exerted significant effects on maintaining the levels of FBG and insulin, and ameliorated the increased levels of TG, TC and LDL-C induced by T2DM. Moreover, apoptosis in liver tissue was relieved by G-Rh1, according to histological analysis. Particularly, in diabetic mice, it was observed that not only the increased secretion of G6Pase and PEPCK in the gluconeogenesis pathway, but also inflammatory factors including NF-κB and NLRP3 were suppressed by G-Rh1 treatment. Furthermore, the underlying mechanisms by which G-Rh1 exhibited ameliorative effects was associated with its capacity to inhibit the activation of the Akt/FoxO1 signaling pathway induced by T2DM. Taken together, our preliminary study demonstrated the potential mechnism of G-Rh1 in protecting the liver against T2DM-induced damage.
Insights
Ginsenoside Rh1 (G-Rh1) protects against type 2 diabetes (T2DM)-induced liver injury by regulating glucose and lipid metabolism and inhibiting inflammation. This compound shows potential for treating diabetes-associated liver damage.
Area of Science:
- Hepatology
- Endocrinology
- Pharmacology
Background:
- Diabetes-associated liver injury is a growing global health concern.
- Type 2 diabetes mellitus (T2DM) significantly contributes to liver damage and failure.
- Effective therapeutic strategies for T2DM-induced hepatopathy are urgently needed.
Purpose of the Study:
- To investigate the protective effects of ginsenoside Rh1 (G-Rh1) against liver injury in a mouse model of T2DM.
- To elucidate the underlying mechanisms of G-Rh1's ameliorative actions on T2DM-induced liver damage.
Main Methods:
- A T2DM mouse model was established using high-fat diet (HFD) and streptozotocin.
- Mice were treated with G-Rh1 (5 and 10 mg·kg⁻¹).
- Evaluated effects on fasting blood glucose (FBG), insulin, lipid profiles (TG, TC, LDL-C), liver histology, gluconeogenic enzymes (G6Pase, PEPCK), inflammatory factors (NF-κB, NLRP3), and the Akt/FoxO1 signaling pathway.
Main Results:
- G-Rh1 treatment maintained normal FBG and insulin levels.
- G-Rh1 ameliorated elevated TG, TC, and LDL-C levels.
- Histological analysis revealed reduced liver apoptosis.
- G-Rh1 suppressed gluconeogenesis (G6Pase, PEPCK) and inflammation (NF-κB, NLRP3).
- G-Rh1 inhibited T2DM-induced activation of the Akt/FoxO1 signaling pathway.
Conclusions:
- Ginsenoside Rh1 demonstrates significant protective effects against T2DM-induced liver injury.
- G-Rh1 acts by modulating glucose and lipid metabolism, reducing inflammation, and inhibiting the Akt/FoxO1 pathway.
- G-Rh1 shows potential as a therapeutic agent for managing diabetes-associated liver disease.
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