Luteolin ameliorates cardiac failure in type I diabetic cardiomyopathy

Wang, Guo Guang; Li, Wei; Lü, Xiaohua; Bao, Pengju; Zhang, Xue

doi:10.1016/j.jdiacomp.2012.04.007

Cited by 66 publications

(43 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several mitochondria (M) exhibited swelling, fusion and disruption of cristae, and thinning of the Z lines were observed in the untreated diabetic group. Long-term treatment with genistein significantly improved these morphological changes animals [9,10]. Oxidative stress is an imbalance between oxidants, such as ROS and antioxidants, and probably contributes to the development, progression, and complications of diabetes [10].…”

Section: Discussionmentioning

confidence: 99%

“…The important role of growth factors in pathogenesis of longterm complications of diabetes was suggested by their increased concentrations in target tissue [9]. Ample evidence demonstrates elevated TGF-b1 expression during the transition from stable hypertrophy to heart failure in both experimental models and human heart failure [21,46].…”

Section: Discussionmentioning

confidence: 99%

“…The increased levels of oxidative stress caused by imbalance between the generation of reactive oxygen species (ROS) and endogenous reserve of antioxidants, result in initiation and progression of cardiac dysfunction, remodeling of the extracellular matrix in the heart, and culminating in oxidative myocardial injury [9,10].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Genistein ameliorates cardiac inflammation and oxidative stress in streptozotocin-induced diabetic cardiomyopathy in rats

et al. 2015

View full text Add to dashboard Cite

The present study was undertaken to evaluate the protective effects of genistein against cardiac inflammation and oxidative stress in streptozotocin (STZ) (45 mg/kg body weight)-induced diabetic rats. genistein (300 mg/kg/day) was administered orally for 24 weeks to STZ-induced diabetic rats. The effects of genistein on blood glucose, % glycosylated hemoglobin (HbA1c), C-reactive protein, tumor necrosis factor (TNF- α), transforming growth factor (TGF-β1), and total antioxidant were studied. Ultrastructural and histopathological assessment of injury were also undertaken using transmission electron microscope. STZ-induced diabetes resulted in significant increase in the levels of blood glucose, HbA1c, C-reactive protein, TNF- α and TGF-β1, and a decline in total antioxidant reserve of the myocardium. Administration of genistein to diabetic rats resulted in a decrease in blood glucose (p< 0.001), % HbA1c (p < 0.0001), C-reactive protein (p < 0.001), and expression of TNF- α (p < 0.001) and TGF-β1 (p < 0.0001) proteins. In addition, genistein treatment results in augmentation of total antioxidant (p < 0.01) reserve of the hearts. The above findings were supported by histological as well as immunohistochemical localization of NF-κB (p65) in the heart. Genistein treatment ameliorated the ultrastructural degenerative changes in the cardiac tissues as compared to the diabetic control. The result demonstrates that genistein restored the integrity of the diabetic myocardium by virtue of its anti-inflammatory and antioxidant effects.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Genistein ameliorates cardiac inflammation and oxidative stress in streptozotocin-induced diabetic cardiomyopathy in rats

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Luteolin or its conjugate reduced plasma LDL and TC in diabetic rats (Wang et al, 2012) and normal adult rats (Azevedo et al, 2010), and elevated HDL levels in the study by Wang et al (2012). The flavone also prevents lipid accumulation in cultured hepatic cells (Liu et al, 2011).…”

Section: Discussionmentioning

confidence: 76%

Coadministrating Luteolin Minimizes the Side Effects of the Aromatase Inhibitor Letrozole

Wong

Lin

et al. 2014

The Journal of Pharmacology and Experimental Therapeutics

View full text Add to dashboard Cite

Aromatase inhibitors (AIs) have been used as adjuvant therapeutic agents for breast cancer. Their adverse side effect on blood lipid is well documented. Some natural compounds have been shown to be potential AIs. In the present study, we compared the efficacy of the flavonoid luteolin to the clinically approved AI letrozole (Femara; Novartis Pharmaceuticals, East Hanover, NJ) in a cell and a mouse model. In the in vitro experimental results for aromatase inhibition, the K i values of luteolin and letrozole were estimated to be 2.44 mM and 0.41 nM, respectively. Both letrozole and luteolin appeared to be competitive inhibitors. Subsequently, an animal model was used for the comparison. Aromataseexpressing MCF-7 cells were transplanted into ovariectomized athymic mice. Luteolin was given by mouth at 5, 20, and 50 mg/kg, whereas letrozole was administered by intravenous injection. Similar to letrozole, luteolin administration reduced plasma estrogen concentrations and suppressed the xenograft proliferation. The regulation of cell cycle and apoptotic proteins-such as a decrease in the expression of Bcl-xL, cyclin-A/D1/E, CDK2/4, and increase in that of Bax-was about the same in both treatments. The most significant disparity was on blood lipids. In contrast to letrozole, luteolin increased fasting plasma high-density lipoprotein concentrations and produced a desirable blood lipid profile. These results suggested that the flavonoid could be a coadjuvant therapeutic agent without impairing the action of AIs.

show abstract

“…In rat models of streptozotocin-induced type 1 diabetes, LU administration has been reported to reduce blood glucose levels [31] and ameliorate diabetic cardiomyopathy [32] and nephropathy [31], suggesting its potency in improving glucose and lipid metabolism in animals. In addition, LU supplementation in mice fed with an HFD during the establishment of DIO has previously been reported to protect the animals from HFD-induced insulin resistance [15].…”

Section: Discussionmentioning

confidence: 99%

Luteolin reduces obesity-associated insulin resistance in mice by activating AMPKα1 signalling in adipose tissue macrophages

et al. 2016

View full text Add to dashboard Cite

Aims/hypothesis Inflammatory polarisation of adipose tissue macrophages (ATMs) plays a critical role in the development of obesity-associated metabolic diseases such as insulin resistance and diabetes. Our previous study indicated that dietary luteolin (LU) could prevent the establishment of insulin resistance in mice fed a high-fat diet (HFD). Here, we further investigated the effects of LU, which is a natural flavonoid, on pre-established insulin resistance and obesityassociated ATM polarisation in mice. Methods Five-week-old C57/BL6 mice were fed on a low-fat diet or HFD for 20 weeks, with some mice receiving supplementation with 0.01% LU from weeks 1 or 10 of the HFD to assess the actions of LU on insulin resistance and ATM polarisation. Furthermore, the role of LU in metabolicdysfunction-associated macrophage phenotypes was investigated in vitro. Results Dietary LU supplementation, either for 20 weeks or from weeks 10 to 20 of an HFD, significantly improved insulin resistance in HFD-fed mice. In addition, inflammatory macrophage infiltration and polarisation were suppressed in mouse epididymal adipose tissues. Furthermore, LU treatment directly reversed lipopolysaccharide-stimulated and metabolism-regulated molecules, and induced inflammatory polarisation in mouse RAW264.7 cells and peritoneal cavity resident macrophages. Finally, using the selective AMPactivated protein kinase (AMPK) inhibitor compound C and Ampkα1 (also known as Prkaa1) silencing with siRNA, we found that LU activated AMPKα1 in macrophages to inhibit their inflammatory polarisation and enhanced insulin signals in adipocytes that were stimulated with macrophageconditioned media. Conclusions/interpretation Dietary LU ameliorated insulin resistance in diet-induced obese mice by promoting AMPKα1 signalling in ATMs.

show abstract

Luteolin ameliorates cardiac failure in type I diabetic cardiomyopathy

Cited by 66 publications

References 45 publications

Genistein ameliorates cardiac inflammation and oxidative stress in streptozotocin-induced diabetic cardiomyopathy in rats

Genistein ameliorates cardiac inflammation and oxidative stress in streptozotocin-induced diabetic cardiomyopathy in rats

Coadministrating Luteolin Minimizes the Side Effects of the Aromatase Inhibitor Letrozole

Luteolin reduces obesity-associated insulin resistance in mice by activating AMPKα1 signalling in adipose tissue macrophages

Contact Info

Product

Resources

About