scholarly journals The Molecular Mechanism of Protective Effects of Grape Seed Proanthocyanidin Extract on Reperfusion Arrhythmias in Rats in Vivo

2010 ◽  
Vol 33 (5) ◽  
pp. 759-767 ◽  
Author(s):  
Gaixia Zhao ◽  
Haiqing Gao ◽  
Jie Qiu ◽  
Weida Lu ◽  
Xinbing Wei
Keyword(s):  
Molecular Mechanism ◽  
Grape Seed ◽  
Protective Effects ◽  
Reperfusion Arrhythmias ◽  
Grape Seed Proanthocyanidin Extract ◽  
Grape Seed Proanthocyanidin

scholarly journals Grape Seed Proanthocyanidin Extract Ameliorates Cardiac Remodelling After Myocardial Infarction Through PI3K/AKT Pathway in Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Yongxue Ruan ◽  
Qike Jin ◽  
Jingjing Zeng ◽  
Fangfang Ren ◽  
Zuoyi Xie ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Dysfunction ◽  
Grape Seed ◽  
Akt Pathway ◽  
Grape Seeds ◽  
Hypoxic Conditions ◽  
Grape Seed Proanthocyanidin Extract ◽  
Grape Seed Proanthocyanidin

Myocardial infarction is one of the most serious fatal diseases in the world, which is due to acute occlusion of coronary arteries. Grape seed proanthocyanidin extract (GSPE) is an active compound extracted from grape seeds that has anti-oxidative, anti-inflammatory and anti-tumor pharmacological effects. Natural products are cheap, easy to obtain, widely used and effective. It has been used to treat numerous diseases, such as cancer, brain injury and diabetes complications. However, there are limited studies on its role and associated mechanisms in myocardial infarction in mice. This study showed that GSPE treatment in mice significantly reduced cardiac dysfunction and improved the pathological changes due to MI injury. In vitro, GSPE inhibited the apoptosis of H9C2 cells after hypoxia culture, resulting in the expression of Bax decreased and the expression of Bcl-2 increased. The high expression of p-PI3K and p-AKT was detected in MI model in vivo and in vitro. The use of the specific PI3K/AKT pathway inhibitor LY294002 regressed the cardio-protection of GSPE. Our results showed that GSPE could improve the cardiac dysfunction and remodeling induced by MI and inhibit cardiomyocytes apoptosis in hypoxic conditions through the PI3K/AKT signaling pathway.

scholarly journals Grape Seed Proanthocyanidin Extract Prevents Ovarian Aging by Inhibiting Oxidative Stress in the Hens

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Xingting Liu ◽  
Xin Lin ◽  
Yuling Mi ◽  
Jian Li ◽  
Caiqiao Zhang
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Chromatin Condensation ◽  
Natural Aging ◽  
Grape Seed ◽  
Protective Effects ◽  
Ovarian Aging ◽  
Grape Seed Proanthocyanidin Extract ◽  
Age Related ◽  
Grape Seed Proanthocyanidin

Oxidative stress is an important inducement in ovarian aging which results in fecundity decline in human and diverse animals. As a potent antioxidant, grape seed proanthocyanidin extract (GSPE) was investigated to ameliorate chicken ovarian aging in this study. Firstly, ovarian antioxidant capacity of hens at different ages (90, 150, 280, and 580 days old) was compared to elucidate its age-related changes. Subsequently, a D-gal-induced (2.5 mg/mL) aging ovarian model was established and the cultured ovarian tissues were treated with GSPE at 5 μg/mL for 72 h to evaluate the putative attenuating effects of GSPE on ovarian aging. Meanwhile, ovaries of D280 (young) and D580 (old) were treated with GSPE for 72 h in culture to verify the protective effects of GSPE on natural aging ovary. The results showed that GSPE could rescue the antioxidant capacity decline by increasing the antioxidase activities and their gene expression in either D-gal-induced or natural aging ovaries. Moreover, GSPE could maintain the homeostasis between cell proliferation and apoptosis in the D-gal-induced and natural aging ovaries, as well as alleviate D-gal-induced nucleus chromatin condensation in the ovarian granulosa cells. In conclusion, GSPE treatment can effectively prevent the ovarian aging process in hens by reducing oxidative stress.

scholarly journals Grape Seed Proanthocyanidin Extract Prevents Bone Loss via Regulation of Osteoclast Differentiation, Apoptosis, and Proliferation

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3164
Author(s):  
Sung Chul Kwak ◽  
Yoon-Hee Cheon ◽  
Chang Hoon Lee ◽  
Hong Young Jun ◽  
Kwon-Ha Yoon ◽  
...  
Keyword(s):  
Bone Loss ◽  
Osteoclast Differentiation ◽  
Grape Seed ◽  
Mitogen Activated Protein Kinase ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Nuclear Factor ◽  
Systemic Injection ◽  
Grape Seed Proanthocyanidin Extract ◽  
Grape Seed Proanthocyanidin

Dietary procyanidin has been shown to be an important bioactive component that regulates various pharmacological activities to maintain metabolic homeostasis. In particular, grape seed proanthocyanidin extract (GSPE) is a commercially available medicine for the treatment of venous and lymphatic dysfunction. This study aimed to investigate whether GSPE protects against lipopolysaccharide (LPS)-induced bone loss in vivo and the related mechanism of action in vitro. The administration of GSPE restored the inflammatory bone loss phenotype stimulated by acute systemic injection of LPS in vivo. GSPE strongly suppressed receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast differentiation and bone resorption activity of mature osteoclasts by decreasing the RANKL-induced nuclear factor-κB transcription activity. GSPE mediates this effect through decreased phosphorylation and degradation of NF-κB inhibitor (IκB) by IκB kinaseβ, subsequently inhibiting proto-oncogene cellular Fos and nuclear factor of activated T cells. Additionally, GSPE promotes osteoclast proliferation by increasing the phosphorylation of components of the Akt and mitogen-activated protein kinase signaling pathways and it also inhibits apoptosis by decreasing the activity of caspase-8, caspase-9, and caspase-3, as corroborated by a decrease in the Terminal deoxynucleotidyl transferase dUTP nick end labeling -positive cells. Our study suggests a direct effect of GSPE on the proliferation, differentiation, and apoptosis of osteoclasts and reveals the mechanism responsible for the therapeutic potential of GSPE in osteoclast-associated bone metabolism disease.

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