Ginsenoside Rb1 Protects Against Diabetic Cardiomyopathy by Regulating the Adipocytokine Pathway

Zhang, Chenyang; Han, Meixin; Zhang, Xuelian; Tong, Hongna; Sun, Xiaobo; Sun, Guibo

doi:10.2147/jir.s348866

Cited by 24 publications

(22 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inflammation is increased in DCM in vitro and vivo, and 6-G treatment reduces this inflammation. This confirms previous studies showing that inflammatory cytokines IL-1 β , IL-6, and TNF- α are elevated in DCM [ 34 , 35 ]. 6-G also has anti-inflammatory effects in other diseases such as sepsis, cerebral ischemia/reperfusion injury, and diabetic nephropathy [ 25 , 36 , 37 ].…”

Section: Discussionsupporting

confidence: 92%

6-Gingerol Alleviates Ferroptosis and Inflammation of Diabetic Cardiomyopathy via the Nrf2/HO-1 Pathway

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

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 μM) and then treated with 6-G (100 μM). 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-1β, 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.

show abstract

Section: Discussionsupporting

confidence: 92%

6-Gingerol Alleviates Ferroptosis and Inflammation of Diabetic Cardiomyopathy via the Nrf2/HO-1 Pathway

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…It has been well established that DCM is attributed to various factors, including hyperglycemia, insulin disorder, inflammation, oxidative stress, cardiomyocyte apoptosis and others [9][10][11]. High glucose may directly mediate proinflammatory factors secretion and perpetuate the inflammatory process, causing cardiomyocyte hypertrophy, mitochondrial dysfunction, endoplasmic reticulum stress and death, fibroblast proliferation, collagen production and then promoting the development of DCM [12].…”

Section: Introductionmentioning

confidence: 99%

Dihydromyricetin Attenuates Diabetic Cardiomyopathy by Inhibiting Oxidative Stress, Inflammation and Necroptosis via Sirtuin 3 Activation

et al. 2023

View full text Add to dashboard Cite

Dihydromyricetin (DHY), the main flavonoid component in Ampelopsis grossedentata, has important benefits for health. The present study aimed to investigate the exact effects and possible mechanisms of DHY on diabetic cardiomyopathy (DCM). Male C57BL/6 mice and sirtuin 3 (SIRT3) knockout (SIRT3-KO) mice were injected with streptozotocin (STZ) to induce a diabetic model. Two weeks later, DHY (250 mg/kg) or carboxymethylcellulose (CMC) were administrated once daily by gavage for twelve weeks. We found that DHY alleviated fasting blood glucose (FBG) and triglyceride (TG) as well as glycosylated hemoglobin (HbA1c) levels; increased fasting insulin (FINS); improved cardiac dysfunction; ameliorated myocardial hypertrophy, fibrosis and injury; suppressed oxidative stress, inflammasome and necroptosis; but improved SIRT3 expression in STZ-induced mice. Neonatal rat cardiomyocytes were pre-treated with DHY (80 μM) with or without high glucose (HG) stimulation. The results showed that DHY attenuated cell damage but improved SIRT3 expression and inhibited oxidative stress, inflammasome and necroptosis in cardiomyocytes with high glucose stimulation. Moreover, the above protective effects of DHY on DCM were unavailable in SIRT3-KO mice, implying a promising medical potential of DHY for DCM treatment. In sum, DHY improved cardiac dysfunction; ameliorated myocardial hypertrophy, fibrosis and injury; and suppressed oxidative stress, inflammation and necroptosis via SIRT3 activation in STZ-induced diabetic mice, suggesting DHY may serve as a candidate for an agent to attenuate diabetic cardiomyopathy.

show abstract

“…The results showed that ginsenoside Rb1 attenuated the levels of CRP, MCP-1, IL-1β, IL-6, and TNF-α in serum. This work demonstrated that ginsenoside Rb1 ameliorated MIRI of diabetic animals by regulating adipocytokine pathway and antioxidant pathway 35 . The left coronary artery of SD rats was occluded for 45 min followed by reperfusion for 2 h. Ginsenoside Rb1 showed a protective effect against MIRI.…”

Section: Ginsenoside Rb1mentioning

confidence: 67%

The Role of Ginsenosides in Myocardial Ischemic Injury-A Systematic Review

Wang¹,

Fu²,

Zhang³

2022

Asian J Pharm Res Dev

View full text Add to dashboard Cite

Topical herbal formulations are gaining more attention in wound healing due to their safety and efficacy. This is a systematic review of the effects of Curcuma longatopical formulations on wound healing. C. longa is a traditional medicinal plant used due to its antimicrobial, antioxidant, anti-inflammatory, and wound healing properties. Studies carried outas randomized control trials and clinical trials were included for the analysis of this review. Searches were conducted in PubMed, Scopus, Cochrane Central Register of Controlled Trials, and Google scholar (up to March 2022) with 04 studies meeting the inclusion criteria. All randomized control trials and clinical trials have shown a significant improvement in wound healing. The topical formulations containing C. longa as an ingredient have reportedly improved wound healing in cases of eczema, radiodermatitis, acne vulgaris, atopic dermatitis, ichthyosis vulgaris, senile pruritis, and xerotic skin conditions, according to the studies covered in this review.This review identified some evidence that C. longa extract has good effects for wound healing, in accordance with its use in traditional medicine. To evaluate the impact of C. longa on wound healing, including complications, larger, well-designed randomized control trials are required.

show abstract

Ginsenoside Rb1 Protects Against Diabetic Cardiomyopathy by Regulating the Adipocytokine Pathway

Cited by 24 publications

References 38 publications

6-Gingerol Alleviates Ferroptosis and Inflammation of Diabetic Cardiomyopathy via the Nrf2/HO-1 Pathway

6-Gingerol Alleviates Ferroptosis and Inflammation of Diabetic Cardiomyopathy via the Nrf2/HO-1 Pathway

Dihydromyricetin Attenuates Diabetic Cardiomyopathy by Inhibiting Oxidative Stress, Inflammation and Necroptosis via Sirtuin 3 Activation

The Role of Ginsenosides in Myocardial Ischemic Injury-A Systematic Review

Contact Info

Product

Resources

About