20(S)-ginsenoside Rh1 alleviates T2DM induced liver injury via the Akt/FOXO1 pathway.
10.1016/S1875-5364(22)60201-2
- Author:
Wen-Ya SU
1
;
Mei-Ling FAN
2
;
Ying LI
1
;
Jun-Nan HU
1
;
En-Bo CAI
1
;
Hong-Yan ZHU
1
;
Ming-Jie SONG
3
,
4
;
Wei LI
3
,
5
Author Information
1. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
2. Maternity Diagnosis & Treatment Center, the Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 130021, China.
3. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China
4. National & Local Joint Engineering Research Center for Ginseng Breeding and Development, Changchun 130118, China. Electronic address: songmingjie2017@126.com.
5. National & Local Joint Engineering Research Center for Ginseng Breeding and Development, Changchun 130118, China. Electronic address: liwei7727@126.com.
- Publication Type:Journal Article
- Keywords:
Akt/FOXO1;
G-Rh1;
G6Pase;
Gluconeogenesis;
Inflammation;
Liver injury;
PEPCK
- MeSH:
Animals;
Chemical and Drug Induced Liver Injury, Chronic;
Cholesterol, LDL/pharmacology*;
Diabetes Mellitus, Experimental/metabolism*;
Diabetes Mellitus, Type 2/metabolism*;
Forkhead Box Protein O1/pharmacology*;
Ginsenosides;
Insulin/metabolism*;
Liver;
Mice;
Mice, Inbred C57BL;
NF-kappa B/metabolism*;
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism*;
Proto-Oncogene Proteins c-akt/metabolism*;
Streptozocin
- From:
Chinese Journal of Natural Medicines (English Ed.)
2022;20(9):669-678
- CountryChina
- Language:English
-
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.
