ReferenceID 4409
6-Gingerol Alleviates Ferroptosis and Inflammation of Diabetic Cardiomyopathy via the Nrf2/HO-1 Pathway
Oxid Med Cell Longev
Background: Diabetes mellitus (DM) can induce cardiomyocyte injury and lead to diabetic cardiomyopathy (DCM) which presently has no specific treatments and consequently increase risk of mortality. Objective: To character
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- Reference Id
- 4409
- Evidence Id
- 20999
- Core Evidence Id
- 20999
- Source Reference Id
- 2106
- Herb2 Reference Id
- HBREF002903
- Subject Paper Key
- HBIN012366_36624878
- Pubmed Id
- 36624878
- Doi
- 10.1155/2022/3027514
- Paper Title
- 6-Gingerol Alleviates Ferroptosis and Inflammation of Diabetic Cardiomyopathy via the Nrf2/HO-1 Pathway
- Paper Abstract
- Background: Diabetes mellitus (DM) can induce cardiomyocyte injury and lead to diabetic cardiomyopathy (DCM) which presently has no specific treatments and consequently increase risk of mortality. Objective: To characterize the therapeutic effect of 6-gingerol (6-G) on DCM and identify its potential mechanism. Methods: In vivo streptozotocin- (STZ-) induced DM model was established by using a high-fat diet and STZ, followed by low-dose (25 mg/kg) and high-dose (75 mg/kg) 6-G intervention. For an in vitro DCM model, H9c2 rat cardiomyoblast cells were stimulated with high glucose (glucose = 33 mM) and palmitic acid (100 μ M) and then treated with 6-G (100 μ M). Histological and echocardiographic analyses were used to assess the effect of 6-G on cardiac structure and function in DCM. Western blotting, ELISA, and real-time qPCR were used to assess the expression of ferroptosis, inflammation, and the Nrf2/HO-1 pathway-related proteins and RNAs. Protein expression of collagen I and collagen III was assessed by immunohistochemistry, and kits were used to assay SOD, MDA, and iron levels. Results: The results showed that 6-G decreased cardiac injury in both mouse and cell models of DCM. The cardiomyocyte hypertrophy and interstitial fibrosis were attenuated by 6-G treatment in vivo and resulted in an improved heart function. 6-G inhibited the expression of ferroptosis-related protein FACL4 and the content of iron and enhanced the expression of anti-ferroptosis-related protein GPX4. In addition, 6-G also diminished the secretion of inflammatory cytokines, including IL-1 β , IL-6, and TNF- α . 6-G treatment activated the Nrf2/HO-1 pathway, enhanced antioxidative stress capacity proved by increased activity of SOD, and decreased MDA production. Compared with in vivo, 6-G treatment of H9c2 cells treated with high glucose and palmitic acid could produce a similar effect. Conclusion: These findings suggest that 6-G could protect against DCM by the mechanism of ferroptosis inhibition and inflammation reduction via enhancing the Nrf2/HO-1 pathway.
- Journal
- Oxid Med Cell Longev
- Publish Year
- 2023
- Experiment Subject
- mouse; rat; h9c2 cells; h9c2 rat cardiomyoblast cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Cardiomyocyte Injury; Interstitial Fibrosis; Diabetes Mellitus; Cardiomyocyte Hypertrophy; Diabetic Cardiomyopathy
- Paper Title Cn
- Paper Title En
- 6-Gingerol Alleviates Ferroptosis and Inflammation of Diabetic Cardiomyopathy via the Nrf2/HO-1 Pathway
- Bilingual Status
- semi_complete