Aqueous extract of Houttuynia cordata ameliorates aortic endothelial injury during hyperlipidemia via FoxO1 and p38 MAPK pathway

Publication date: November 2019Source: Journal of Functional Foods, Volume 62Author(s): Xuyun Liu, Ke Cao, Weiqiang Lv, Jing Liu, Jing Gao, Yan Wang, Chuan Qin, Jianshu Liu, Weijin Zang, Jiankang LiuAbstractIncreasing evidence demonstrates that hyperlipidemia plays a causal role in the development of cardiovascular diseases (CVDs) due to endothelial dysfunction. Houttuynia cordata aqueous extract (HAE), using as both medicine and food, whose effect and mechanism were investigated in endothelial dysfunction. In vivo, it profoundly attenuated hyperlipidemia-induced accumulation of serum metabolites, which in turn contributed to alleviating morphologic and functional damage in vascular endothelium. Moreover, the decrease expression of FoxO1/PGC-1α and mitochondrial complexes in thoracic vessels were ameliorated by HAE administration. Through in vitro cultures, consistently, the results showed that HAE predominantly activated PGC-1α for mitochondrial biogenesis via enhancing FoxO1 expression. Additionally, silencing of FoxO1 remarkably abolished the ability of HAE to augment PGC-1α expression, implying the imperative role of FoxO1 during protection. Besides, the anti-inflammation was mainly mediated via p38 MAPK pathway. Briefly, our study demonstrated that HAE ameliorated hyperlipidemia-induced endothelial injury via upregulating FoxO1/PGC-1α and suppressing p38 MAPK.Graphical abstract
Source: Journal of Functional Foods - Category: Nutrition Source Type: research

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Authors: Caparros Lefebvre D Abstract In the 90's, clinico pathological studies have considerably improved the diagnosis of specific and rare neurodegenerative diseases. After a training in Parkinsons' disease in Paris, the author moved to French West Indies (Guadeloupe) and observed a high incidence of atypical parkinsonism with dementia, unresponsive to levodopa. Similar features were observed in Martinique. An environmental origin has been suspected with the exposure to toxins of annonaceae leaves and seeds. The candidate toxins are acetogenins acting as mitochondrial poison. This was demonstrated in neuronal ce...
Source: Revue Neurologique - Category: Neurology Tags: Rev Neurol (Paris) Source Type: research
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Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs
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Source: Mitochondrion - Category: Biochemistry Source Type: research
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Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
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Source: Oncology Letters - Category: Cancer & Oncology Tags: Oncol Lett Source Type: research
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Source: Molecular Genetics and Metabolism - Category: Genetics & Stem Cells Source Type: research
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Source: Journal of Neurochemistry - Category: Neuroscience Authors: Tags: Original Article Source Type: research
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Source: Mitochondrion - Category: Biochemistry Source Type: research
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Source: Biochimica et Biophysica Acta (BBA) Biomembranes - Category: Biochemistry Source Type: research
Background: Reversing or preventing T-cell exhaustion is an important treatment goal in the context of HIV disease; however, the mechanisms that regulate HIV-specific CD8+ T-cell exhaustion are incompletely understood. Since mitochondrial mass (MM), mitochondrial membrane potential (MMP), and cellular reactive oxygen species (ROS) content are altered in exhausted CD8+ T cells in other settings, we hypothesized that similar lesions may arise in HIV infection. Methods: We sampled cryopreserved peripheral blood mononuclear cells from HIV-uninfected (n = 10) and HIV-infected participants with varying levels and mechanisms...
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